151 results on '"Catherine Vergely"'
Search Results
2. Does size matter? Focus on the impact of reducing litter size in mice on cardio-metabolic risk and cardiac sensitivity to in vivo ischemia in adulthood
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Eve Rigal, Marie Josse, Geoffrey Dogon, Luc Rochette, Charles Guenancia, and Catherine Vergely-Vandriesse
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Cardiology and Cardiovascular Medicine - Published
- 2023
3. Plasma growth differentiation factor − 8 / Myostatin level as prognostic biomarker of patients with ischemic stroke and acute revascularization therapy. PARADISE study
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Pauline Jakubina, Alexandre Meloux, Gauthier Duloquin, Serge Aho, Catherine Vergely, and Yannick Béjot
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Neurology ,Neurology (clinical) - Published
- 2023
4. Influence of postnatal overfeeding on postnatal heart development in juvenile mice
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Marie Josse, Eve Rigal, Nathalie Rosenblatt-Velin, Francesca Rochais, Geoffrey Dogon, Luc Rochette, Marianne Zeller, and Catherine Vergely
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Cardiology and Cardiovascular Medicine - Published
- 2023
5. Growth differentiation factor 15 (GDF15) preconditioning but not post-conditioning protects the hearts towards ischemia-reperfusion injury
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Geoffrey Dogon, Eve Rigal, Marie Josse, Luc Rochette, Yannick Bejot, and Catherine Vergely
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Cardiology and Cardiovascular Medicine - Published
- 2023
6. Stress: Eight Decades after Its Definition by Hans Selye: 'Stress Is the Spice of Life'
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Luc Rochette, Geoffrey Dogon, and Catherine Vergely
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General Neuroscience - Abstract
July 1936: Hans Selye describes in 74 lines in the prestigious journal Nature a new concept: Stress [...]
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- 2023
7. Multimodal approach for the prediction of atrial fibrillation detected after stroke: SAFAS study
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Lucie Garnier, Gauthier Duloquin, Alexandre Meloux, Karim Benali, Audrey Sagnard, Mathilde Graber, Geoffrey Dogon, Romain Didier, Thibaut Pommier, Catherine Vergely, Yannick Béjot, and Charles Guenancia
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Cardiology and Cardiovascular Medicine - Abstract
BackgroundIntensive screening for atrial fibrillation (AF) has led to a better recognition of this cause in stroke patients. However, it is currently debated whether AF Detected After Stroke (AFDAS) has the same pathophysiology and embolic risk as prior-to-stroke AF. We thus aimed to systematically approach AFDAS using a multimodal approach combining clinical, imaging, biological and electrocardiographic markers.MethodsPatients without previously known AF admitted to the Dijon University Hospital (France) stroke unit for acute ischemic stroke were prospectively enrolled. The primary endpoint was the presence of AFDAS at 6 months, diagnosed through admission ECG, continuous electrocardiographic monitoring, long-term external Holter during the hospital stay, or implantable cardiac monitor if clinically indicated after discharge.ResultsOf the 240 included patients, 77 (32%) developed AFDAS. Compared with sinus rhythm patients, those developing AFDAS were older, more often women and less often active smokers. AFDAS patients had higher blood levels of NT-proBNP, osteoprotegerin, galectin-3, GDF-15 and ST2, as well as increased left atrial indexed volume and lower left ventricular ejection fraction. After multivariable analysis, galectin-3 ≧ 9 ng/ml [OR 3.10; 95% CI (1.03–9.254), p = 0.042], NT-proBNP ≧ 290 pg/ml [OR 3.950; 95% CI (1.754–8.892, p = 0.001], OPG ≥ 887 pg/ml [OR 2.338; 95% CI (1.015–5.620), p = 0.046) and LAVI ≥ 33.5 ml/m2 [OR 2.982; 95% CI (1.342–6.625), p = 0.007] were independently associated with AFDAS.ConclusionA multimodal approach combining imaging, electrocardiography and original biological markers resulted in good predictive models for AFDAS. These results also suggest that AFDAS is probably related to an underlying atrial cardiopathy.Clinical Trial Registration[www.ClinicalTrials.gov], identifier [NCT03570060].
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- 2023
8. Involvement of Oxidative Stress in Protective Cardiac Functions of Calprotectin
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Luc, Rochette, Geoffrey, Dogon, Eve, Rigal, Marianne, Zeller, Yves, Cottin, and Catherine, Vergely
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Inflammation ,Oxidative Stress ,S100 Proteins ,Alarmins ,Calgranulin B ,Humans ,Calgranulin A ,Leukocyte L1 Antigen Complex - Abstract
Calprotectin (CLP) belonging to the S-100 protein family is a heterodimeric complex (S100A8/S100A9) formed by two binding proteins. Upon cell activation, CLP stored in neutrophils is released extracellularly in response to inflammatory stimuli and acts as damage-associated molecular patterns (DAMPs). S100A8 and S100A9 possess both anti-inflammatory and anti-bacterial properties. The complex is a ligand of the toll-like receptor 4 (TLR4) and receptor for advanced glycation end (RAGE). At sites of infection and inflammation, CLP is a target for oxidation due to its co-localization with neutrophil-derived oxidants. In the heart, oxidative stress (OS) responses and S100 proteins are closely related and intimately linked through pathophysiological processes. Our review summarizes the roles of S100A8, S100A9 and CLP in the inflammation in relationship with vascular OS, and we examine the importance of CLP for the mechanisms driving in the protection of myocardium. Recent evidence interpreting CLP as a critical modulator during the inflammatory response has identified this alarmin as an interesting drug target.
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- 2022
9. Role of humanin, a mitochondrial-derived peptide, in cardiovascular disorders
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Alexandre Meloux, Luc Rochette, Catherine Vergely, Yves Cottin, Marianne Zeller, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), and Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC)
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Cell ,Peptide ,030204 cardiovascular system & hematology ,Mitochondrion ,medicine.disease_cause ,Cardiovascular System ,03 medical and health sciences ,0302 clinical medicine ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Animals ,Humans ,Medicine ,030212 general & internal medicine ,Endothelial dysfunction ,ComputingMilieux_MISCELLANEOUS ,Humanin ,chemistry.chemical_classification ,business.industry ,Intracellular Signaling Peptides and Proteins ,General Medicine ,medicine.disease ,Mitochondria ,Up-Regulation ,Cell biology ,Oxidative Stress ,Open reading frame ,medicine.anatomical_structure ,chemistry ,Cardiovascular Diseases ,Inflammation Mediators ,Cardiology and Cardiovascular Medicine ,business ,Function (biology) ,Oxidative stress ,Signal Transduction - Abstract
The mitochondria produce specific peptides-mitochondrial-derived peptides-that mediate the transcriptional stress response by their translocation into the nucleus and interaction with deoxyribonucleic acid. Mitochondrial-derived peptides are regulators of metabolism. This class of peptides comprises humanin, mitochondrial open reading frame of the 12S ribosomal ribonucleic acid type c (MOTS-c) and small humanin-like peptides (SHLPs). Humanin inhibits mitochondrial complex 1 activity and limits the level of oxidative stress in the cell. Data show that mitochondrial-derived peptides have a role in improving metabolic diseases, such as type 2 diabetes. Perhaps humanin can be used as a marker for mitochondrial function in cardiovascular disease or as a pharmacological strategy in patients with endothelial dysfunction. The goal of this review is to discuss the newly emerging functions of humanin, and its biological role in cardiovascular disorders.
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- 2020
10. Assessment of Clinical Scales for Detection of Large Vessel Occlusion in Ischemic Stroke Patients from the Dijon Stroke Registry
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Gauthier Duloquin, Mathilde Graber, Lucie Garnier, Sophie Mohr, Maurice Giroud, Catherine Vergely, and Yannick Béjot
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large vessel occlusion ,ischemic stroke ,scales ,Medicine ,registry ,population studies ,General Medicine ,Article - Abstract
(1) Background: The limited availability of thrombectomy-capable stroke centres raises questions about pre-hospital triage of patients with suspected stroke (IS) due to large vessel occlusion (LVO). Aims: This study aimed to evaluate the diagnostic accuracy of clinical stroke severity scales available for LVO detection. (2) Methods: Patients with IS were prospectively identified among residents of Dijon, France, using a population-based registry (2013–2017). Clinical signs and arterial imaging data were collected. LVO was defined as an occlusion site affecting the terminal intracranial internal carotid artery, the M1 segment of the middle cerebral artery (MCA), or the basilar artery (restricted definition). A wide definition of LVO also included the M2 segment of the MCA. For each of the 16 evaluated scales, a receiver operator characteristic (ROC) analysis was performed, and the c-statistic representing the area under the ROC curve was evaluated to assess discrimination for predicting LVO. (3) Results: 971 patients were registered, including 123 patients (12.7%) with an LVO according to the restricted definition. The c-statistic for LVO detection ranged between 0.66 and 0.80 according to the different scales, with a sensibility varying from 70% to 98% and a specificity from 33% to 86%. According to the wide definition of LVO (174 patients, 17.9%), the c-statistic was slightly lower, ranging between 0.64 and 0.79. The sensitivity was 59% to 93%, and the specificity was 34% to 89%. (4) Conclusion: The clinical scales failed to combine a high sensitivity and a high specificity to detect LVO. Further studies are needed to determine the best strategy for pre-hospital triage of IS patients.
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- 2021
11. Pre-existing brain damage and association between severity and prior cognitive impairment in ischemic stroke patients
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Valentin Pinguet, Gauthier Duloquin, Thomas Thibault, Hervé Devilliers, Pierre-Olivier Comby, Valentin Crespy, Frédéric Ricolfi, Catherine Vergely, Maurice Giroud, and Yannick Béjot
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Radiological and Ultrasound Technology ,Radiology, Nuclear Medicine and imaging ,Neurology (clinical) - Abstract
We evaluated whether pre-existing brain damage may explain greater severity in cognitively-impaired patients with ischemic stroke (IS).IS patients were retrieved from the population-based registry of Dijon, France. Pre-existing damage (leukoaraiosis, old vascular brain lesions, cortical and central brain atrophy) was assessed on initial CT-scan. Association between prestroke cognitive status defined as no impairment, mild cognitive impairment (MCI), or dementia, and clinical severity at IS onset assessed with the NIHSS score was evaluated using ordinal regression analysis. Mediation analysis was performed to assess pre-existing brain lesions as mediators of the relationship between cognitive status and severity.Among the 916 included patients (mean age 76.8 ± 15.0 years, 54.3% women), those with pre-existing MCI (n = 115, median NIHSS [IQR]: 6 [2-15]) or dementia (n = 147, median NIHSS: 6 [3-15]) had a greater severity than patients without (n = 654, median NIHSS: 3 [1-9]) in univariate analysis (OR=1.69; 95% CI: 1.18-2.42, p = 0.004, and OR=2.06; 95% CI: 1.49-2.84, p 0.001, respectively). Old cortical lesion (OR=1.53, p = 0.002), central atrophy (OR=1.41, p = 0.005), cortical atrophy (OR=1.90, p 0.001) and moderate (OR=1.41, p = 0.005) or severe (OR=1.84, p = 0.002) leukoaraiosis were also associated with greater severity. After adjustments, pre-existing MCI (OR=1.52; 95% CI: 1.03-2.26, p = 0.037) or dementia (OR=1.94; 95% CI: 1.32-2.86, p = 0.001) remained associated with higher severity at IS onset, independently of confounding factors including imaging variables. Association between cognitive impairment and severity was not mediated by pre-existing visible brain damages.Impaired brain ischemic tolerance in IS patients with prior cognitive impairment could involve other mechanisms than pre-existing visible brain damage.
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- 2021
12. Lipid Peroxidation and Iron Metabolism: Two Corner Stones in the Homeostasis Control of Ferroptosis
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Luc Rochette, Geoffrey Dogon, Eve Rigal, Marianne Zeller, Yves Cottin, and Catherine Vergely
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Inorganic Chemistry ,Organic Chemistry ,General Medicine ,Physical and Theoretical Chemistry ,Molecular Biology ,Spectroscopy ,Catalysis ,Computer Science Applications - Abstract
Regulated cell death (RCD) has a significant impact on development, tissue homeostasis, and the occurrence of various diseases. Among different forms of RCD, ferroptosis is considered as a type of reactive oxygen species (ROS)-dependent regulated necrosis. ROS can react with polyunsaturated fatty acids (PUFAs) of the lipid (L) membrane via the formation of a lipid radical L• and induce lipid peroxidation to form L-ROS. Ferroptosis is triggered by an imbalance between lipid hydroperoxide (LOOH) detoxification and iron-dependent L-ROS accumulation. Intracellular iron accumulation and lipid peroxidation are two central biochemical events leading to ferroptosis. Organelles, including mitochondria and lysosomes are involved in the regulation of iron metabolism and redox imbalance in ferroptosis. In this review, we will provide an overview of lipid peroxidation, as well as key components involved in the ferroptotic cascade. The main mechanism that reduces ROS is the redox ability of glutathione (GSH). GSH, a tripeptide that includes glutamic acid, cysteine, and glycine, acts as an antioxidant and is the substrate of glutathione peroxidase 4 (GPX4), which is then converted into oxidized glutathione (GSSG). Increasing the expression of GSH can inhibit ferroptosis. We highlight the role of the xc- GSH-GPX4 pathway as the main pathway to regulate ferroptosis. The system xc-, composed of subunit solute carrier family members (SLC7A11 and SLC3A2), mediates the exchange of cystine and glutamate across the plasma membrane to synthesize GSH. Accumulating evidence indicates that ferroptosis requires the autophagy machinery for its execution. Ferritinophagy is used to describe the removal of the major iron storage protein ferritin by the autophagy machinery. Nuclear receptor coactivator 4 (NCOA4) is a cytosolic autophagy receptor used to bind ferritin for subsequent degradation by ferritinophagy. During ferritinophagy, stored iron released becomes available for biosynthetic pathways. The dysfunctional ferroptotic response is implicated in a variety of pathological conditions. Ferroptosis inducers or inhibitors targeting redox- or iron metabolism-related proteins and signal transduction have been developed. The simultaneous detection of intracellular and extracellular markers may help diagnose and treat diseases related to ferroptotic damage.
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- 2022
13. Exogenous growth differentiation factor 15 (GDF15) exerts direct cardioprotective properties towards myocardial ischemia reperfusion injury
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Geoffrey Dogon, Eve Rigal, Luc Rochette, Yannick Bejot, and Catherine Vergely
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Cardiology and Cardiovascular Medicine - Published
- 2022
14. Mitochondrial-derived peptides: New markers for cardiometabolic dysfunction
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Luc Rochette, Eve Rigal, Geoffrey Dogon, Gabriel Malka, Marianne Zeller, Catherine Vergely, and Yves Cottin
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Oxidative Stress ,Cardiovascular Diseases ,Humans ,General Medicine ,Cardiology and Cardiovascular Medicine ,Peptides ,Biomarkers ,Mitochondria - Abstract
Great attention is being paid to the evaluation of new markers in blood circulation for the estimation of tissue metabolism disturbance. This endogenous disturbance may contribute to the onset and progression of cardiometabolic disease. In addition to their role in energy production and metabolism, mitochondria play a main function in cellular mechanisms, including apoptosis, oxidative stress and calcium homeostasis. Mitochondria produce mitochondrial-derived peptides that mediate the transcriptional stress response by translocating into the nucleus and interacting with deoxyribonucleic acid. This class of peptides includes humanin, mitochondrial open reading frame of the 12S ribosomal ribonucleic acid type c (MOTS-c) and small humanin-like peptides. Mitochondrial-derived peptides are regulators of metabolism, exerting cytoprotective effects through antioxidative stress, anti-inflammatory responses and antiapoptosis; they are emerging biomarkers reflecting mitochondrial function, and the circulating concentration of these proteins can be used to diagnose cardiometabolic dysfunction. The aims of this review are: (1) to describe the emerging role for mitochondrial-derived peptides as biomarkers; and (2) to discuss the therapeutic application of these peptides.
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- 2021
15. The Role of Osteoprotegerin in Vascular Calcification and Bone Metabolism: The Basis for Developing New Therapeutics
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Luc Rochette, Eve Rigal, Marianne Zeller, Gabriel Malka, Yves Cottin, Catherine Vergely, Alexandre Meloux, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), and Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC)
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musculoskeletal diseases ,0301 basic medicine ,Endocrinology, Diabetes and Metabolism ,Osteoporosis ,030209 endocrinology & metabolism ,Inflammation ,Bone and Bones ,Bone remodeling ,03 medical and health sciences ,0302 clinical medicine ,Endocrinology ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Osteoprotegerin ,medicine ,Animals ,Humans ,Orthopedics and Sports Medicine ,Vascular Calcification ,Receptor ,ComputingMilieux_MISCELLANEOUS ,biology ,business.industry ,Therapies, Investigational ,medicine.disease ,3. Good health ,Cardiovascular Diseases ,RANKL ,Cancer research ,biology.protein ,Tumor necrosis factor alpha ,Bone Remodeling ,030101 anatomy & morphology ,medicine.symptom ,business ,Signal Transduction ,Calcification - Abstract
Osteoporosis (OP) and cardiovascular diseases (CVD) are both important causes of mortality and morbidity in aging patients. There are common mechanisms underlying the regulation of bone remodeling and the development of smooth muscle calcification; a temporal relationship exists between osteoporosis and the imbalance of mineral metabolism in the vessels. Vascular calcification appears regulated by mechanisms that include both inductive and inhibitory processes. Multiple factors are implicated in both bone and vascular metabolism. Among these factors, the superfamily of tumor necrosis factor (TNF) receptors including osteoprotegerin (OPG) and its ligands has been established. OPG is a soluble decoy receptor for receptor activator of nuclear factor-kB ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). OPG binds to RANKL and TRAIL, and inhibits the association with their receptors, which have been labeled as the receptor activator of NF-kB (RANK). Sustained release of OPG from vascular endothelial cells (ECs) has been demonstrated in response to inflammatory proteins and cytokines, suggesting that OPG/RANKL/RANK system plays a modulatory role in vascular injury and inflammation. For the development of potential therapeutic strategies targeting vascular calcification, critical consideration of the implications for bone metabolism must be taken into account to prevent potentially detrimental effects to bone metabolism.
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- 2019
16. Difficultés et besoins des familles d’enfants en rémission d’un cancer pédiatrique
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Astrid de Laage and Catherine Vergely
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medicine.medical_specialty ,Action (philosophy) ,Childhood cancer ,medicine ,Psychiatry ,Psychology ,Pediatrics ,Period (music) - Abstract
Childhood cancer causes immense upheaval for the child and his or her family. The end of the treatments constitutes a transition period which brings with it numerous other problems. It is essential to take into account the difficulties expressed by families and to envisage areas of action to help and support them.
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- 2019
17. Long-term impact of postnatal overfeeding on sensitivity to ischemia-reperfusion injury in vivo and on cardio-metabolism risk
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Eve Rigal, Marie Josse, Geoffrey Dogon, Ivan Porcherot, Luc Rochette, Charles Guenancia, and Catherine Vergely
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Cardiology and Cardiovascular Medicine - Published
- 2022
18. Effect of acute iron infusion on insulin secretion: A randomized, double-blind, placebo-controlled trial
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Evrim Jaccard, Kévin Seyssel, Alexandre Gouveia, Catherine Vergely, Laila Baratali, Cédric Gubelmann, Marc Froissart, Bernard Favrat, Pedro Marques-Vidal, Luc Tappy, and Gérard Waeber
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General Medicine ,Inflammation ,Insulin secretion ,Insulin sensitivity ,Iron deficiency ,Iron sufficiency ,Type 2 diabetes - Abstract
Chronic exposure to high iron levels increases diabetes risk partly by inducing oxidative stress, but the consequences of acute iron administration on beta cells are unknown. We tested whether the acute administration of iron for the correction of iron deficiency influenced insulin secretion and the production of reactive oxygen species. Single-center, double-blinded, randomized controlled trial conducted between June 2017 and March 2020. 32 women aged 18 to 47 years, displaying symptomatic iron deficiency without anaemia, were recruited from a community setting and randomly allocated (1:1) to a single infusion of 1000 mg intravenous ferric carboxymaltose (iron) or saline (placebo). The primary outcome was the between group mean difference from baseline to day 28 in first and second phase insulin secretion, assessed by a two-step hyperglycaemic clamp. All analyses were performed by intention to treat. This trial was registered in ClinicalTrials.gov NCT03191201. Iron infusion did not affect first and second phase insulin release. For first phase, the between group mean difference from baseline to day 28 was 0 μU × 10 min/mL [95% CI, -22 to 22, P = 0.99]. For second phase, it was -5 μUx10min/mL [95% CI, -161 to 151; P = 0.95] at the first plateau of the clamp and -249 μUx10min/mL [95% CI, -635 to 137; P = 0.20] at the second plateau. Iron infusion increased serum ascorbyl/ascorbate ratio, a marker of plasma oxidative stress, at day 14, with restoration of normal ratio at day 28 relative to placebo. Finally, high-sensitive C-reactive protein levels remained similar among groups. In iron deficient women without anaemia, intravenous administration of 1000 mg of iron in a single sitting did not impair glucose-induced insulin secretion despite a transient increase in the levels of circulating reactive oxygen species. The Swiss National Science Foundation, University of Lausanne and Leenaards, Raymond-Berger and Placide Nicod Foundations.
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- 2022
19. Echocardiographic measurement of left ventricular function following myocardial infarction in adult postnatally overfed mice
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Marie Josse, Eve Rigal, Geoffrey Dogon, Ivan Porcherot, Luc Rochette, Marianne Zeller, and Catherine Vergely
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Cardiology and Cardiovascular Medicine - Published
- 2022
20. Evaluation of left ventricular function following myocardial infarction in adult postnatally overfed mice
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I. Porcherot, M. Josse, Eve Rigal, G. Dogon, Marianne Zeller, Catherine Vergely-Vandriesse, and Luc Rochette
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Cardiac function curve ,medicine.medical_specialty ,business.industry ,Diastole ,medicine.disease ,Brain natriuretic peptide ,medicine.anatomical_structure ,Ventricle ,Heart failure ,Internal medicine ,Troponin I ,cardiovascular system ,medicine ,Cardiology ,Myocardial infarction ,Cardiology and Cardiovascular Medicine ,business ,Artery - Abstract
Introduction Perinatal environment, such as nutritional state, is of major importance for short- and long-term cardio-metabolic status. Postnatal overfeeding (PNOF) induced in rodents by litter size reduction at birth reproduces the effects of childhood overnutrition and was shown to affect the cardiovascular function and to predispose to cardiovascular pathologies. The aim of our work was to follow the evolution of cardiac function for 28 days after in vivo myocardial infarction in control or PNOF mice. Method C57BL/6 male mice were raised in litter adjusted to 9 or 3 pups for control and PNOF group respectively. After weaning, mice of both groups had free access to standard diet and water. At 4 months, they were subjected to permanent ligation of the left anterior descending artery (LAD) to induce myocardial infarction or to sham surgery. Echocardiographic measurements were acquired at baseline and 1, 7, 15 and 28 days after surgery for cardiac function evaluation. Twenty-eight days after surgery, the left ventricle (LV) and lungs were weighed and infarct size was assessed. Results At basal state, no difference of cardiac function was observed between the 4 groups. In both control and PNOF mice subjected to LAD ligation, the fractional area change (FAC) was significantly decreased 24 h after surgery and the systolic/diastolic LV area was significantly increased 7 d after surgery, and both remained stable until 28 d. However, no differences neither in LV contractile function nor in infarct size were noticed between control and PNOF mice, except for an increased LV mass in PNOF mice. Conclusion While all groups of mice subjected to myocardial infarction developed heart failure, as demonstrated by decreased LV contractility and dilation, there were no differences between control and PNOF groups. Further measures will be done in order to assess circulating biomarkers as cardiac troponin I (cTnI), brain natriuretic peptide (BNP) and growth differentiation factor-15 (GDF-15).
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- 2021
21. Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways
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Christian Juvet, Benazir Siddeek, Catherine Yzydorczyk, Catherine Vergely, Katya Nardou, Jean-Baptiste Armengaud, Mohamed Benahmed, Umberto Simeoni, François Cachat, Hassib Chehade, Université de Lausanne = University of Lausanne (UNIL), Laboratoire de Physiopathologie et Pharmacologie Cardio-Métaboliques (U866, Lipides et nutrition, équipe 5) (LPPCM), Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), Vergely, Catherine, and Université de Lausanne (UNIL)
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0301 basic medicine ,Senescence ,kidney ,medicine.medical_specialty ,Physiology ,Renal function ,030204 cardiovascular system & hematology ,programming ,[SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology ,lcsh:Physiology ,03 medical and health sciences ,overnutrition ,0302 clinical medicine ,Overnutrition ,Physiology (medical) ,Internal medicine ,Lactation ,medicine ,Weaning ,Original Research ,2. Zero hunger ,Kidney ,postnatal overfeeding ,lcsh:QP1-981 ,biology ,Sirtuin 1 ,medicine.disease ,[SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and Nephrology ,chronic kidney disease ,developmental origins of health and disease ,[SDV.AEN] Life Sciences [q-bio]/Food and Nutrition ,030104 developmental biology ,medicine.anatomical_structure ,Endocrinology ,biology.protein ,[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition ,Kidney disease - Abstract
Background: Early nutrition influences the risk of Chronic Kidney Diseases development in adulthood. Mechanisms underlying the early programming of altered renal function remain incompletely understood. This study aims at characterizing the role of cell senescence pathways in early programming of Chronic Kidney Disease after transient postnatal overfeeding. Material and Methods: Reduced litters of 3 mice pups and standard litters of 10 mice pups were obtained to induce overfed animals during lactation and control animals, respectively. Animals were sacrificed at 24 days (weaning) or at 7 months of life (adulthood). Body weight, blood pressure, kidney weight, and glomerular count were assessed in both groups. Senescence pathways were investigated using β-Galactosidase staining and Western blotting of P16, P21, P53, P-Rb/Rb and Sirtuin 1 proteins. Results: Early overfed animals had a higher body weight, a higher blood pressure at adulthood, and a higher glomerular number endowment compared to the control group. A higher β-Galactosidase activity, a significant increase in P53 protein expression (p=0.0045) and a significant decrease in P-Rb/Rb ratio (p= 0.02), were observed at weaning in animals who underwent early postnatal overfeeding. Protein expression of Sirtuin 1, a protective factor against accelerated stress-induced senescence, was significantly decreased (p=0.03) at weaning in early overfed animals; Conclusion: Early postnatal overfeeding by litter size reduction is associated with increased expression of factors involved in cellular senescence pathways, and decreased expression of Sirt 1 in the mouse kidney at weaning. These alterations may contribute to chronic kidney disease programming after early postnatal overfeeding.
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- 2020
22. Functional roles of GDF15 in modulating microenvironment to promote carcinogenesis
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Marianne Zeller, Catherine Vergely, Alexandre Meloux, Luc Rochette, and Yves Cottin
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0301 basic medicine ,Growth Differentiation Factor 15 ,Angiogenesis ,Carcinogenesis ,Population ,Smad Proteins ,Disease ,medicine.disease_cause ,03 medical and health sciences ,0302 clinical medicine ,Neoplasms ,Glial cell line-derived neurotrophic factor ,medicine ,Tumor Microenvironment ,Humans ,Obesity ,education ,Receptor ,Cyclic AMP Response Element-Binding Protein ,Molecular Biology ,Inflammation ,education.field_of_study ,biology ,Neovascularization, Pathologic ,NF-kappa B ,Gene Expression Regulation, Neoplastic ,Crosstalk (biology) ,030104 developmental biology ,030220 oncology & carcinogenesis ,biology.protein ,Cancer research ,Molecular Medicine ,GDF15 ,Signal Transduction - Abstract
Obesity and related metabolic dysregulation are risk factors for many types of cancer. The interactions between a developing tumor and its microenvironment are known to implicate a complex "crosstalk" among the factors produced by the population of cells. Among these factors, Growth and differentiation factor 15 (GDF15) has a functional role in cancer. GDF15 expression is induced in response to the conditions associated with cellular stress and diseases. The GDF15 receptor, a member of the glial-cell-derived neurotropic factor family (GDNF), is a GDNF family receptor α-like (GFRAL) protein. GDF15 induces pro-angiogenic effects in tumors. However, GDF15 could affect tumorigenesis both positively and negatively. With a better understanding of the upstream disease pathways reflected by GDF15, new treatment targets may emerge.
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- 2019
23. P4573In patients with acute myocardial infarction, PCSK9 levels do not predict severity and recurrence of cardiovascular events
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B. Mouhat, Catherine Vergely, Luc Rochette, Yves Cottin, Gilles Lambert, Michel Farnier, Maud Maza, and Marianne Zeller
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medicine.medical_specialty ,business.industry ,PCSK9 ,Internal medicine ,Cardiology ,Medicine ,Myocardial infarction ,Cardiology and Cardiovascular Medicine ,business ,medicine.disease - Abstract
Background In patients with coronary artery disease (CAD), it remains unclear whether serum PCSK9 levels can predict the severity of the disease and the risk of future cardiovascular events. Methods Among the patients admitted for an acute myocardial infarction (MI) from September 2015 to December 2016 in an intensive care unit from a university hospital, serum PCSK9 levels were measured on admission in patients not previously receiving statin therapy. We aimed to evaluate the association between PCSK9 levels, metabolic parameters, severity of CAD on coronary angiography, and the risk of in-hospital events and at one-year follow-up. Results In a total of 648 patients (mean age: 66 years, 67% male), the median PCSK9 was 263 ng/ml, higher for females compared with males (270 vs 256 ng/ml, p=0.009). Serum PCSK9 was associated with LDL cholesterol (r=0.083, p=0.036), total cholesterol (r=0.136, p=0.001) and triglycerides (r=0.137, p=0.001). A positive association was also observed in the subgroup of patients with CRP >10 mg/L (p Conclusion In this large cohort of patients hospitalized for acute MI and not previously receiving statin therapy, PCSK9 levels was not associated with the severity or the recurrence of cardiovascular events. The clinical utility of measuring PCSK9 levels remains to be demonstrated for this category of patients.
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- 2019
24. P4613Long-term impact of postnatal nutritional programming on cardiac sensitivity to ischemia-reperfusion injury in vivo and on cardio-protective pathways in mice
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I. Porcherot, Catherine Vergely, Eve Rigal, Luc Rochette, C Greco, and Alexandre Meloux
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medicine.medical_specialty ,business.industry ,Cardio protective ,Ischemia ,Infarction ,medicine.disease ,Overnutrition ,Reperfusion therapy ,In vivo ,Internal medicine ,Cardiology ,medicine ,Cardiology and Cardiovascular Medicine ,business ,Ligation ,Reperfusion injury - Abstract
Introduction Nutritional disturbances during the postnatal period may be responsible for a predisposition, or “programming”, to increased cardio-metabolic risk and to a progressive alteration of left ventricular contractility in adulthood. This nutritional perinatal programming may also lead to an alteration of cellular pathways involved in cardiac protection, such as the specific RISK and SAFE pathways, highlighted during pre- and post-ischemic conditioning or those of sirtuins (SIRT), histone deacetylases involved in the regulation of essential biological process. Purpose Our aim was to evaluate in mice the impact of postnatal overfeeding (PNOF) on cardiac sensitivity to ischemia-reperfusion (I-R) injury in vivo and on the myocardial expression of genes involved in heart protection against ischemia. Methods PNOF was induced by the reduction of litter size of C57/BL6 mice immediately after birth: normally-fed group (NF) was composed of 9 male pups/mother and overfed group (OF) of 3 pups/mother. In vivo ischemia-reperfusion injury was induced by the ligation of the anterior interventricular artery for 45 minutes followed by 24 h of reperfusion in hearts from 6-months aged mice. The gene expressions of proteins of interest composing the cardioprotective pathways (RISK pathway: Akt, ERK; SAFE pathway: JAK/STAT3; Sirtuins: SIRT1) were measured by RT-qPCR in mice aged 4 and 6 months. Results PNOF induced in OF group an early and permanent increase in body weight (+23%, p Conclusion Nutritional programming through short-term PNOF induced a long-lasting decrease in the expression of signaling pathways involved in cardiac cellular protection, which could explain why 6-months old mice show increased susceptibility to myocardial I-R injury in vivo. The mechanism of these alterations needs further exploration, but could involve alterations in cardiomyocyte's balance between apoptotic and regenerative pathways, and epigenetic modifications. Acknowledgement/Funding French Fundation
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- 2019
25. P4550Growth differentiation factor 15 as an integrative biomarker of heart failure in patients with acute myocardial infarction
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Alexandre Meloux, Frédéric Chagué, Maud Maza, Marianne Zeller, Florence Bichat, Catherine Vergely, Yves Cottin, and Luc Rochette
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medicine.medical_specialty ,business.industry ,Internal medicine ,Heart failure ,medicine ,Cardiology ,Biomarker (medicine) ,In patient ,Myocardial infarction ,Cardiology and Cardiovascular Medicine ,business ,medicine.disease - Abstract
Background Growth differentiation factor 15 (GDF15), a stress-responsive cytokine member of the transforming growth factor-β family, is an emerging biomarker in cardiovascular (CV) diseases. GDF15 is weakly expressed in normal condition but increased in pathological situations such as inflammation, oxidative stress, and left ventricular remodeling. Recent data suggest GDF15 as a marker in heart failure (HF). Purpose We aimed to identify the determinants of GDF15 circulating levels in patients admitted for an acute myocardial infarction (AMI). Methods In our prospective study, all consecutive patients admitted from June 2016 to February 2018 for type 1 AMI in the Coronary Care unit from our University Hospital were included. Chronic HF patients were excluded. In-hospital severe HF was defined as killip class>2. Blood samples were taken on admission and serum levels of GDF15 were measured using a commercially available ELISA kit. Results Among the 284 AMI patients, median age was at 67 (57–78) y, 27% were women, 23% had diabetes and 59% were hypertensive. GDF15 levels (median = 1,144 (775–1,891) ng/L were strongly correlated with age (r=0.493, p3 mg/L (p5,000 ng/L [OR: 8.43; 95% CI (1.57–45.32)] is as independent estimate of HF, beyond age and other confounding (i.e. admission systolic blood pressure, LVEF and Log N-terminal pro-Brain Natriuretic Peptide). GDF15 levels according to HF development Conclusions These preliminary results suggest that GDF15 could be an integrative biomarker of severe HF in patient with AMI. Further studies are needed to elucidate the underlying mechanisms linking the cytokine with the development of HF.
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- 2019
26. The role of osteoprotegerin in the crosstalk between vessels and bone: Its potential utility as a marker of cardiometabolic diseases
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Yves Cottin, Luc Rochette, Eve Rigal, Catherine Vergely, Alexandre Meloux, Marianne Zeller, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), and Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC)
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musculoskeletal diseases ,0301 basic medicine ,medicine.medical_specialty ,Osteoporosis ,Inflammation ,Disease ,030204 cardiovascular system & hematology ,Bone remodeling ,03 medical and health sciences ,0302 clinical medicine ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Osteoprotegerin ,Internal medicine ,medicine ,Humans ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Pharmacology (medical) ,Vascular Calcification ,Receptor ,Pharmacology ,biology ,Chemistry ,medicine.disease ,3. Good health ,030104 developmental biology ,Endocrinology ,Cardiovascular Diseases ,RANKL ,biology.protein ,Tumor necrosis factor alpha ,Bone Remodeling ,medicine.symptom - Abstract
International audience; Among the numerous molecules that are being studied for their potential utility as biomarkers of cardiovascular diseases, much interest has been shown in the superfamily of tumor necrosis factor (TNF) receptors. Members of this family include osteoprotegerin (OPG) and its ligands, which are receptor activators of nuclear factor κB ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). These signals may be expressed and regulated, and their functions could be involved in several physiological and pathological processes. The relationship between bone regulatory proteins and vascular biology has attracted attention, and it has been suggested that OPG may mediate vascular calcification and cardiometabolic diseases. OPG is steadily released from vascular endothelial cells in response to inflammatory stimuli, suggesting that it plays a modulatory role in vascular injury, inflammation, and atherosclerosis. Vascular calcification, a hallmark of atherosclerosis, is similar to bone remodeling. It is an actively regulated mechanism that includes both inductive and inhibitory processes. There is a temporal link between the development of osteoporosis and vascular calcification, which is particularly marked in post-menopausal women and the elderly. The precise nature of the link between bone metabolism, vascular calcification and cardiovascular disease is largely unknown but increasing evidence suggests that the triad of RANK/RANKL/OPG may be important in the initiation of various diseases. An increased release of OPG is associated with increased cardiovascular risk and it is suggested that increased OPG levels resulting from vascular damage correspond to a protective mechanism. Circulating OPG levels could be used as independent biomarkers of cardiovascular disease in patients with acute or chronic cardiometabolic disease and thus an improved prognosis
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- 2018
27. Growth Differentiation Factor-15 (GDF-15) Is Associated With Mortality in Ischemic Stroke Patients Treated With Acute Revascularization Therapy
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Céline Brenière, Alexandre Méloux, Martin Pédard, Christine Marie, Pierre Thouant, Catherine Vergely, Yannick Béjot, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), and Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC)
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thrombolysis ,medicine.medical_specialty ,medicine.medical_treatment ,Context (language use) ,Disease ,030204 cardiovascular system & hematology ,Revascularization ,Logistic regression ,lcsh:RC346-429 ,03 medical and health sciences ,0302 clinical medicine ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Internal medicine ,medicine ,Stroke ,ComputingMilieux_MISCELLANEOUS ,lcsh:Neurology. Diseases of the nervous system ,Original Research ,business.industry ,Confounding ,Thrombolysis ,medicine.disease ,stroke ,mortality ,3. Good health ,GDF15 ,Neurology ,thrombectomy ,Neurology (clinical) ,business ,030217 neurology & neurosurgery - Abstract
Background and Aims: Growth differentiation factor-15 (GDF-15) has been identified as a robust marker of developing cardiovascular disease, however, little is currently known about its prognostic value in stroke patients. In a context of growing interest to discover new biomarkers in stroke, we aimed to assess the association between circulating GDF-15 levels and three-month mortality in ischemic stroke patients treated with acute revascularization therapy.Methods: 173 patients hospitalized for acute ischemic stroke and treated with either intravenous thrombolysis (n = 99, 57.2%), mechanical thrombectomy (n = 41, 23.4%) or combined therapy (n = 33, 19.1%) were prospectively included. Baseline clinical and biological characteristics were recorded. Plasma GDF-15 levels were measured at admission (D0), and at 24 h, 3 and 7 days. Clinical severity was assessed with the National Institutes of Health Stroke Scale (NIHSS) score, and vital status was obtained 3 months after the stroke.Results: At 3 months post-stroke, 32 patients (18.5%) had died. The deceased patients had higher D0 plasma GDF-15 levels (median [IQR]: 2,777 [1,769–5,446] vs. 1,460 [965–2,079] pg/mL, P < 0.001). In multivariable logistic regression analysis, D0 GDF-15 levels in the third tertile of the distribution were independently associated with mortality at 3 months (OR = 3.71; 95% CI: 1.09–12.6, P = 0.036), even after adjustment for confounding variables including clinical severity.Conclusions: Our data show for the first time that GDF-15 plasma concentration at admission is independently associated with 3-month mortality in ischemic stroke patients treated with acute revascularization therapy. The pathophysiological mechanisms that could explain this association warrant further study.
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- 2019
28. Cerebral microbleeds: A clinical issue for cardiologists?
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Catherine Vergely, Yannick Béjot, Benoit Daubail, Maurice Giroud, Yves Cottin, Gwendoline Dupont, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Registre Dijonnais des Accidents Vasculaires Cérébraux (AVC) - Dijon Stroke Registry, Centre d'épidémiologie des populations ( CEP ), Université de Bourgogne ( UB ) -Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc ( CRLCC - CGFL ) -Université de Bourgogne ( UB ) -Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc ( CRLCC - CGFL ) -Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ), Lipides - Nutrition - Cancer (U866) ( LNC ), Université de Bourgogne ( UB ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon ( ENSBANA ), Service de Cardiologie [CHU de Dijon], Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ), Centre d'épidémiologie des populations (CEP), Université de Bourgogne (UB)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Université de Bourgogne (UB)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), and Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)
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medicine.medical_specialty ,[ SDV.MHEP.AHA ] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO] ,prevalence ,030204 cardiovascular system & hematology ,ischemic-stroke ,03 medical and health sciences ,Cardiologists ,0302 clinical medicine ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Internal medicine ,Basal ganglia ,[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO] ,Humans ,Medicine ,brain microbleeds ,oral anticoagulants ,risk-factors ,Stroke ,cognitive function ,ComputingMilieux_MISCELLANEOUS ,Cerebral Hemorrhage ,Intracerebral hemorrhage ,rotterdam scan ,medicine.diagnostic_test ,business.industry ,ages-reykjavik ,Anticoagulants ,Magnetic resonance imaging ,Atrial fibrillation ,General Medicine ,medicine.disease ,Magnetic Resonance Imaging ,intracerebral hemorrhage ,3. Good health ,Clinical Practice ,atrial-fibrillation ,Intracerebral haemorrhage ,Ischemic stroke ,Cardiology ,Cardiology and Cardiovascular Medicine ,business ,Cerebral microbleeds ,030217 neurology & neurosurgery ,Gradient echo - Abstract
IF 2.271; International audience; Some advances in technologies can help clinicians to better understand diseases and to modify their attitude towards management of their patients in terms of therapeutic strategies. Cerebral microbleeds (CMBs) are recently discovered lesions that have had a significant effect on neurologists' conceptions about cerebral vasculopathies, and about which many questions still need to be answered for clinical practice.CMBs were first described in the 1990s, after the development of magnetic resonance imaging (MRI) sequences called gradient echo T2*. CMBs appear as small round hypointense lesions with a black appearance and a diameter of
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- 2016
29. Growth and differentiation factor 11 (GDF11): Functions in the regulation of erythropoiesis and cardiac regeneration
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Luc Rochette, Yves Cottin, Catherine Vergely, Marianne Zeller, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Laboratoire de Physiopathologie et Pharmacologie Cardio-Métaboliques (U866, Lipides et nutrition, équipe 5) (LPPCM), Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), Vergely, Catherine, and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement
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medicine.medical_specialty ,Smad2 Protein ,Protein Serine-Threonine Kinases ,030204 cardiovascular system & hematology ,Biology ,03 medical and health sciences ,0302 clinical medicine ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Internal medicine ,TGF beta signaling pathway ,[SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology ,medicine ,Humans ,Regeneration ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Pharmacology (medical) ,Phosphorylation ,CCL11 ,Activin type 2 receptors ,030304 developmental biology ,Pharmacology ,0303 health sciences ,R-SMAD ,cardiac regeneration ,Growth differentiation factor ,Heart ,Activins ,[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Cell biology ,BMPR2 ,Growth Differentiation Factors ,Endocrinology ,Bone Morphogenetic Proteins ,GDF11 ,Signal transduction ,Activin Receptors, Type I ,erythropoiesis ,ACVR2B ,Signal Transduction - Abstract
International audience; Members of the TGF-β superfamily transduce their signals through type I and II receptor serine/threonine kinases. The binding of activins to activin type IIA (ActRIIA) or type IIB (ActRIIB) receptors induces the recruitment and phosphorylation of an activin type I receptor (ALK4 and/or ALK7), which then phosphorylates the Smad2 and Smad3 intracellular signaling proteins. The regulation of members of the TGF-β family is known to be complex, because many proteins able to bind the ligands and inhibit their activities have been identified. Growth and differentiation factor 11 (Gdf11) belongs to the TGF-β family. GDF11, like other members of the TGF-β superfamily, is produced from precursor proteins by proteolytic processing. Recent studies have reported that GDF11-ActRIIB-Smad2/3-dependent signaling is a key regulatory mechanism in proliferating erythroid precursors as it controls their late-stage maturation. In mammalian tissues, aging is typically accompanied by a progressive loss of homeostasis and impaired regenerative potential. The administration of GDF11 is effective in experimental cardiac hypertrophy, and the identification of GDF11 as a "rejuvenating factor" opens up perspectives for the treatment of age-related cardiac dysfunction. Recent studies of the heart, skeletal muscle and central nervous system indicate that exposure to young blood reverses age-related impairments. The molecular mediators of this "rejuvenation" include growth factors such as GDF11 and cytokines such as CCL11. GDF11 and CCL11 are, perhaps, only the first two in a series of circulating molecules that will be found to influence the aging of different tissues; Are CCL11 and GDF11 endogenous factors for an "elixir of youth"?
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- 2015
30. Low Circulating Levels of Growth Differentiation Factor-15 Before Coronary Artery Bypass Surgery May Predict Postoperative Atrial Fibrillation
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Charles Guenancia, Abdelkader Kahli, Gabriel Laurent, Olivier Bouchot, Charline Pujos, Catherine Vergely, Ghislain Malapert, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Laboratoire de Physiopathologie et Pharmacologie Cardio-Métaboliques (U866, Lipides et nutrition, équipe 5) (LPPCM), Lipides - Nutrition - Cancer (U866) (LNC), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement
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medicine.medical_specialty ,Ejection fraction ,business.industry ,Atrial fibrillation ,EuroSCORE ,medicine.disease ,Amiodarone ,Preoperative care ,3. Good health ,Cardiac surgery ,law.invention ,Coronary artery bypass surgery ,Anesthesiology and Pain Medicine ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,law ,Internal medicine ,Cardiopulmonary bypass ,Cardiology ,Medicine ,Cardiology and Cardiovascular Medicine ,business ,ComputingMilieux_MISCELLANEOUS ,medicine.drug - Abstract
Objectives To assess the role of growth differentiation factor-15 (GDF-15) as a potential new predictor of postoperative atrial fibrillation (POAF) after off-pump (OFP) and on-pump (ONP) coronary artery bypass graft (CABG) surgery. Design Prospective, single-center, observational study. Setting University teaching hospital. Participants The first 50 patients planned for OFP surgery and the first 50 patients planned for ONP surgery among patients referred for CABG with the following exclusion criteria: age 80 years, previous atrial fibrillation/flutter, previous treatment with amiodarone, previous cardiac surgery, and emergency surgery. Interventions Included patients were equipped with long-duration (7 days) Holter-ECG monitoring. Measurements and Main Results POAF was defined as an AF episode lasting>30 seconds. All patients underwent preoperative echocardiography to assess left ventricular ejection fraction and left atrial diameter. GDF-15 levels were assessed after induction of anesthesia and 12 hours after arrival at the intensive care unit. Among the 100 patients, 34 (34%) developed POAF. In Cox multivariate regression analysis, the EuroSCORE, left atrial diameter>45 mm, and low GDF-15 levels at induction were associated independently with the onset of POAF. In contrast, preoperative NT-proBNP levels did not predict POAF. The use of ONP surgery was not associated with a higher incidence of POAF, even though baseline and follow-up characteristics in ONP and OFP patients were identical. Conclusions In patients with no history of AF, a low plasma level of GDF-15 before CABG surgery was a strong independent predictor of POAF. Moreover, preoperative plasma GDF-15 levels added an incremental predictive value to classic risk factors of POAF.
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- 2015
31. Hans Selye and the stress response: 80 years after his 'letter' to the Editor of Nature
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Luc Rochette, Catherine Vergely, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), and Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC)
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0301 basic medicine ,Letter to the editor ,Psychoanalysis ,business.industry ,Fight-or-flight response ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Medicine ,Cardiology and Cardiovascular Medicine ,business ,ComputingMilieux_MISCELLANEOUS ,030217 neurology & neurosurgery - Abstract
International audience
- Published
- 2017
32. La transition de l’enfant atteint de cancer, regard des familles
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Catherine Vergely
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03 medical and health sciences ,medicine.medical_specialty ,0302 clinical medicine ,030220 oncology & carcinogenesis ,medicine ,Cancer ,Psychology ,medicine.disease ,Psychiatry ,Pediatrics ,Family life - Abstract
THE TRANSITION OF CHILDREN AFFECTED BY CANCER, THE FAMILY PERSPECTIVE.: During serious diseases in childhood such as cancer, the journey of the families is staged in information and transition times, which are essential stages for rebuilding family life. Support, orientation and proposals for a way forward are necessary for patients or their families not to be left in destructive isolation. Support actions for patients and their loved ones are implemented, particularly by associations.
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- 2017
33. Implications of excess weight in the cardiotoxicity of anthracyclines and trastuzumab in breast cancer
- Author
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Luc Rochette, Yves Cottin, François Ghiringelli, Catherine Vergely, Sylvain Ladoire, Charles Guenancia, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Lipides - Nutrition - Cancer [Dijon - U1231] (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Service de Cardiologie [CHU de Dijon], Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Département d'oncologie médicale [Centre Georges-François Leclerc], Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER, Equipe CADIR (LNC - U1231), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Lipides - Nutrition - Cancer [Dijon - U1231] ( LNC ), Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ), Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc ( CRLCC - CGFL ), Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM), and Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM)
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0301 basic medicine ,Oncology ,Excess weight ,Anthracycline ,Overweight ,Weight Gain ,Body Mass Index ,Antineoplastic Agents, Immunological ,Breast cancer ,0302 clinical medicine ,Risk Factors ,Trastuzumab ,Medicine ,Anthracyclines ,Disease ,skin and connective tissue diseases ,ComputingMilieux_MISCELLANEOUS ,Trials ,Antibiotics, Antineoplastic ,General Medicine ,[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,3. Good health ,Treatment Outcome ,030220 oncology & carcinogenesis ,Female ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,Doxorubicin-induced cardiotoxicity ,medicine.drug ,Risk ,medicine.medical_specialty ,Heart Diseases ,Breast Neoplasms ,Editorial Material ,03 medical and health sciences ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Internal medicine ,Humans ,Obesity ,Cardiotoxicity ,business.industry ,medicine.disease ,030104 developmental biology ,business - Abstract
International audience; Anthracyclines are anticancer agents with a broad spectrum of activity in oncological practice. However, the use of anthracyclines is limited by the cardiotoxicity they may induce [1]. Following the administration of anthracyclines in the setting of adjuvant therapy for breast cancer, trastuzumab (Herceptin), a humanized monoclonal antibody against the human epidermal growth factor receptor 2 (HER 2) protein, is effective in patients that overexpress this receptor [1]. The addition of trastuzumab therapy to sequential anthracycline and taxane adjuvant treatment reduced the risk of breast cancer recurrence by nearly one-half, and the risk of death by one-third [2]. However, while preclinical studies did not reveal cardiotoxicity, later clinical studies showed that treatment with trastuzumab led to an unexpected incidence of cardiac side-effects [3]. The most frequent effect was reduced systolic ventricular function, asymptomatic or associated with heart failure.
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- 2017
34. Anti-Aging Effects of GDF11 on Skin
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Luc Rochette, Loubna Mazini, Gabriel Malka, Catherine Vergely, Alexandre Meloux, Yves Cottin, Marianne Zeller, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), and Université Mohammed VI Polytechnique
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Aging ,Human skin ,Review ,Skin Aging ,lcsh:Chemistry ,0302 clinical medicine ,Skin Physiological Phenomena ,lcsh:QH301-705.5 ,Spectroscopy ,Skin ,0303 health sciences ,integumentary system ,General Medicine ,3. Good health ,Computer Science Applications ,Cell biology ,Growth Differentiation Factors ,medicine.anatomical_structure ,Bone Morphogenetic Proteins ,Intercellular Signaling Peptides and Proteins ,Disease Susceptibility ,Stem cell ,Signal Transduction ,Biology ,Catalysis ,Inorganic Chemistry ,03 medical and health sciences ,Immune system ,Dermis ,growth factors ,medicine ,Animals ,Humans ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Physical and Theoretical Chemistry ,skin aging ,Molecular Biology ,030304 developmental biology ,Wound Healing ,disease ,Epidermis (botany) ,Regeneration (biology) ,Organic Chemistry ,lcsh:Biology (General) ,lcsh:QD1-999 ,Gene Expression Regulation ,regeneration ,GDF11 ,[SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/Dermatology ,030217 neurology & neurosurgery - Abstract
International audience; Human skin is composed of three layers: the epidermis, the dermis, and the hypodermis. The epidermis has four major cell layers made up of keratinocytes in varying stages of progressive differentiation. Skin aging is a multi-factorial process that affects every phase of its biology and function. The expression profiles of inflammation-related genes analyzed in resident immune cells demonstrated that these cells have a strong ability to regenerate adult skin stem cells and to produce endogenous substances such as growth differentiation factor 11 (GDF11). GDF11 appears to be the key to progenitor proliferation and/or differentiation. The preservation of youthful phenotypes has been tied to the presence of GDF11 in different human tissues, and, in the skin, this factor inhibits inflammatory responses. The protective role of GDF11 depends on a multi-factorial process implicating various types of skin cells such as keratinocytes, fibroblasts and inflammatory cells. GDF11 should be further studied for the purpose of developing novel therapies for the treatment of skin diseases.
- Published
- 2020
35. 1203Post-ischemic stroke-induced myocardial dysfunction is associated with nitro-oxidative stress and sympathetic overactivity
- Author
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Eve Rigal, I. Porcherot, Alexandre Meloux, Yannick Béjot, Yves Cottin, Catherine Vergely, and Luc Rochette
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medicine.medical_specialty ,business.industry ,Internal medicine ,Ischemic stroke ,Cardiology ,medicine ,Nitro ,Cardiology and Cardiovascular Medicine ,medicine.disease_cause ,business ,Oxidative stress - Published
- 2018
36. Transient postnatal over nutrition induces long-term alterations in cardiac NLRP3-inflammasome pathway
- Author
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Na Li, J.-F. Tolsa, Catherine Vergely, Mohamed Benahmed, Claire Mauduit, Umberto Simeoni, Eve Rigal, Hassib Chehade, Catherine Yzydorczyk, Benazir Siddeek, Jean-Baptiste Armengaud, Université de Lausanne = University of Lausanne (UNIL), Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre méditerranéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), and Vergely, Catherine
- Subjects
0301 basic medicine ,Time Factors ,Litter Size ,Inflammasomes ,Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,Medicine (miscellaneous) ,Inflammasome ,Overnutrition ,Insulin ,Nutrition and Dietetics ,integumentary system ,biology ,Micro-RNAs ,Transfection ,[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Animal Nutritional Physiological Phenomena ,Signal transduction ,Cardiology and Cardiovascular Medicine ,medicine.drug ,Signal Transduction ,Cardiac function curve ,medicine.medical_specialty ,Heart Diseases ,Cardiac dysfunctions ,Nutritional Status ,Context (language use) ,Cell Line ,Proto-Oncogene Protein c-ets-1 ,03 medical and health sciences ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Internal medicine ,NLR Family, Pyrin Domain-Containing 3 Protein ,medicine ,Animals ,Post-transcriptional regulation ,Nutrition ,business.industry ,Myocardium ,Rats ,Mice, Inbred C57BL ,Insulin receptor ,Disease Models, Animal ,MicroRNAs ,030104 developmental biology ,Endocrinology ,Animals, Newborn ,biology.protein ,business - Abstract
International audience; Background and aims: The prevalence of obesity is increasing worldwide at an alarming rate. Altered early nutrition, in particular postnatal overfeeding (PNOF), is a risk factor for impaired cardiac function in adulthood. In the understanding of the initiation or progression of heart diseases, NLRP3 inflammasome and non-coding RNAs have been proposed as key players. In this context, the aim of this study was to decipher the role of NLRP3 inflammasome and its post transcriptional control by micro-RNAs in the regulation of cardiac metabolic function induced by PNOF in mice. Methods and results: Based on a model of mice exposed to PNOF through litter size reduction, we observed increased cardiac protein expression levels of NLRP3 and ETS-1 associated with alterations in insulin signaling. Additionally, miR-193b levels were down-regulated in the adult hearts of overfed animals. In a cardiomyocyte cell line, transfection with miR-193b induced down-regulation of ETS-1 and NLRP3 and improved insulin signaling. Conclusions: These findings suggest that the miR-193b could be involved in cardiac phenotypic changes observed in adulthood induced by PNOF likely through the regulation of ETS-1 and NLRP3 expression, and through this of insulin signaling.
- Published
- 2018
37. Growth differentiation factor 15 as an integrative biomarker of heart failure in patients with acute myocardial infarction
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Maud Maza, Frédéric Chagué, Méloux, Luc Rochette, Jean-Claude Beer, Catherine Vergely-Vandriesse, Florence Bichat, Marianne Zeller, and Yves Cottin
- Subjects
medicine.medical_specialty ,Ejection fraction ,business.industry ,030204 cardiovascular system & hematology ,medicine.disease ,03 medical and health sciences ,0302 clinical medicine ,Diabetes mellitus ,Internal medicine ,Heart failure ,medicine ,Cardiology ,Biomarker (medicine) ,cardiovascular diseases ,030212 general & internal medicine ,Myocardial infarction ,GDF15 ,business ,Prospective cohort study ,Cardiology and Cardiovascular Medicine ,Pathological - Abstract
Background Growth differentiation factor 15 (GDF15), a stress-responsive cytokine member of the transforming growth factor-β family, is an emerging biomarker in cardiovascular (CV) diseases. GDF15 is weakly expressed in normal condition but increased in pathological situations such as inflammation, oxidative stress, and left-ventricular remodeling. Recent data suggest GDF15 as a marker in heart failure (HF). Purpose We aimed to measure the levels of GDF15 in patients admitted for an acute myocardial infarction (AMI) and HF. Methods In our prospective study, we included all consecutive patients admitted from June 2016 to October 2017 with type 1 AMI from the ‘obseRvatoire des Infarctus de Cote d’Or’ (RICO) survey. Chronic congestive HF patients were excluded. Admission and hospital HF were diagnosed by killip class > 1. Serum levels of GDF15 were measured using a commercially available ELISA kit. Results Among the 219 AMI patients, median-age was at 69(58–80) y, 29% were women, 25% had diabetes and 63% were hypertensive. GDF15 levels (median = 1254 (819–2140) ng/L) were strongly correlated with age (r = 0.558, P 3 mg/L (P Fig. 1 ). GDF15 levels were negatively correlated with LVEF (r = -0.142, P Conclusions These preliminary results suggest that GDF15 could be an integrative biomarker of HF in patient with AMI. Further studies are needed to elucidate the underlying mechanisms linking the cytokine with the development of HF and to investigate its use for patient monitoring in AMI.
- Published
- 2019
38. Toll-like receptor 5 deficiency exacerbates cardiac injury and inflammation induced by myocardial ischaemia-reperfusion in the mouse
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Pal Pacher, Lucas Liaudet, Catherine Vergely, Bernard Waeber, Na Li, Roumen Parapanov, Jérôme Lugrin, François Feihl, Giuseppina Milano, Nathalie Rosenblatt-Velin, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Laboratoire de Physiopathologie et Pharmacologie Cardio-Métaboliques (U866, Lipides et nutrition, équipe 5) (LPPCM), Lipides - Nutrition - Cancer (U866) (LNC), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bourgogne (UB)-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement
- Subjects
Male ,Chemokine ,medicine.medical_specialty ,Genotype ,p38 mitogen-activated protein kinases ,Myocardial Infarction ,Myocardial Reperfusion Injury ,Inflammation ,030204 cardiovascular system & hematology ,Biology ,p38 Mitogen-Activated Protein Kinases ,Ventricular Function, Left ,Proinflammatory cytokine ,Ventricular Dysfunction, Left ,03 medical and health sciences ,0302 clinical medicine ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Internal medicine ,medicine ,Animals ,Phosphorylation ,Protein kinase B ,030304 developmental biology ,Mice, Knockout ,0303 health sciences ,Toll-like receptor ,Myocardium ,General Medicine ,Immunity, Innate ,3. Good health ,Mice, Inbred C57BL ,Disease Models, Animal ,Oxidative Stress ,Toll-Like Receptor 5 ,CXCL2 ,Phenotype ,Endocrinology ,biology.protein ,TLR4 ,Inflammation Mediators ,medicine.symptom ,Proto-Oncogene Proteins c-akt - Abstract
Myocardial ischaemia-reperfusion (MIR) triggers a sterile inflammatory response important for myocardial healing, but which may also contribute to adverse ventricular remodelling. Such inflammation is initiated by molecular danger signals released by damaged myocardium, which induce innate immune responses by activating toll-like receptors (TLRs). Detrimental roles have been recently reported for TLR2, TLR3 and TLR4. The role of other TLRs is unknown. We therefore evaluated the role of TLR5, expressed at high level in the heart, in the development of myocardial damage and inflammation acutely triggered by MIR. TLR5−/− and wild-type (WT) mice were exposed to MIR (30 min ischaemia, 2 h reperfusion). We measured infarct size, markers of cardiac oxidative stress, myocardial phosphorylation state of mitogen-activated protein (MAP) kinases and AKT, expression levels of chemokines and cytokines in the heart and plasma, as well as cardiac function by echography and conductance volumetry. TLR5-deficient mice had normal cardiac morphology and function under physiological conditions. After MIR, the absence of TLR5 promoted an increase in infarct size and myocardial oxidative stress. Lack of TLR5 fostered p38 phosphorylation, reduced AKT phosphorylation and markedly increased the expression of inflammatory cytokines, whereas it precipitated acute LV (left ventricle) dysfunction. Therefore, contrary to the detrimental roles of TLR2, TLR3 and TLR4 in the infarcted heart, TLR5 is important to limit myocardial damage, inflammation and functional compromise after MIR. Abbreviations: AAR, area at risk; CCL2, chemokine (C-C motif) ligand 2; CXCL2, chemokine (C-X-C motif) ligand 2; DAMP, damage-associated molecular pattern; Ees, end-systolic elastance; EF, ejection fraction; ERK, extracellular signal-regulated kinase; ESPVR, end-systolic pressure-volume relationship; FS, fractional shortening; HNE, hydroxynonenal; HRP, horseradish peroxidase; IL, interleukin; JNK, c-Jun N-terminal kinase; KC, keratinocyte chemoattractant; LV, left ventricle; LVEDD, left ventricle end-diastolic dimension; MAP kinase, mitogen-activated protein kinase; MCP-1, monocyte chemoattractant protein 1; MDA, malondialdehyde; MI, myocardial infarction; MIR, myocardial ischaemia-reperfusion; MyD88, myeloid differentiation primary response gene 88; PBMC, peripheral blood mononuclear cell; Pes, end-systolic pressure; PMN, polymorphonuclear; PV, pressure-volume; TLR, toll-like receptor; Trif, toll-like receptor-associated activator of interferon; TTC, triphenyl tetrazolium chloride; V0, zero pressure intercept; Ved, end-diastolic volume; Ves, end-systolic volume; WT, wild-type
- Published
- 2015
39. Redox Functions of Heme Oxygenase-1 and Biliverdin Reductase in Diabetes
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Luc Rochette, Marianne Zeller, Catherine Vergely, Yves Cottin, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), and Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC)
- Subjects
0301 basic medicine ,Oxygenase ,Oxidoreductases Acting on CH-CH Group Donors ,Bilirubin ,Endocrinology, Diabetes and Metabolism ,medicine.disease_cause ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Endocrinology ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,medicine ,Diabetes Mellitus ,Humans ,Heme ,ComputingMilieux_MISCELLANEOUS ,chemistry.chemical_classification ,Inflammation ,Reactive oxygen species ,Biliverdin ,Chemistry ,Biliverdin reductase ,3. Good health ,Heme oxygenase ,Oxidative Stress ,030104 developmental biology ,Biochemistry ,Oxidation-Reduction ,030217 neurology & neurosurgery ,Oxidative stress ,Heme Oxygenase-1 - Abstract
In patients with diabetes, the hyperglycemia-driven excess generation of reactive oxygen species (ROS) induces oxidative stress (OS) in a variety of tissues. OS is closely associated with chronic inflammation and has a key role in the pathogenesis of vascular complications. The enzymes that generate ROS and gasotransmitters are redox regulated and are implicated in cellular signaling. As a result of cellular metabolism, cells produce significant amounts of carbon monoxide (CO), mainly from heme degradation catalyzed by heme oxygenases (HOs). These reactions also generate biliverdin, bilirubin (BR), and iron. The conversion of biliverdin to BR is catalyzed by biliverdin reductase-A (BVR-A). In this review, we focus on the importance of the HO-1/CO system and BVR in the pathophysiology and therapy of inflammation associated with diabetes.
- Published
- 2017
40. P1742Experimental ischemic stroke in rats induce myocardial contractile dysfunction in vivo and ex vivo and increase cardiac vulnerability to ischemia-reperfusion injury ex vivo
- Author
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Yannick Béjot, Yves Cottin, Luc Rochette, Alexandre Meloux, Eve Rigal, and Catherine Vergely
- Subjects
medicine.medical_specialty ,business.industry ,Ischemia ,medicine.disease ,In vivo ,Internal medicine ,Ischemic stroke ,medicine ,Cardiology ,Medical emergency ,Cardiology and Cardiovascular Medicine ,business ,Reperfusion injury ,Ex vivo - Published
- 2017
41. Transient postnatal overfeeding causes liver stress-induced premature senescence in adult mice
- Author
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Na Li, Mickael Bidho, Katya Nardou, Hassib Chehade, Jean Baptiste Armengaud, Mohamed Benahmed, Umberto Simeoni, Benazir Siddeek, Basile Keshavjee, Dolores Mosig, Catherine Yzydorczyk, Catherine Vergely, Université de Lausanne (UNIL), Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), and Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC)
- Subjects
0301 basic medicine ,Liver Cirrhosis ,Aging ,lcsh:Medicine ,Stress-induced premature senescence ,medicine.disease_cause ,chemistry.chemical_compound ,0302 clinical medicine ,Overnutrition ,Insulin ,lcsh:Science ,2. Zero hunger ,Multidisciplinary ,biology ,Superoxide ,medicine.anatomical_structure ,Liver ,Hepatocyte ,Body Composition ,Female ,Signal Transduction ,Senescence ,Aging/pathology ,Animals ,Animals, Newborn ,Body Weight ,DNA Damage ,Glucose/metabolism ,Glucose Tolerance Test ,Insulin/metabolism ,Liver/metabolism ,Liver/pathology ,Liver Cirrhosis/pathology ,Membrane Transport Proteins/metabolism ,Mice, Inbred C57BL ,Overnutrition/pathology ,Oxidative Stress ,Staining and Labeling ,Stress, Physiological ,medicine.medical_specialty ,030209 endocrinology & metabolism ,Article ,Superoxide dismutase ,03 medical and health sciences ,Insulin resistance ,Internal medicine ,medicine ,lcsh:R ,Membrane Transport Proteins ,[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology ,medicine.disease ,Insulin receptor ,030104 developmental biology ,Endocrinology ,Glucose ,chemistry ,biology.protein ,lcsh:Q ,[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition ,Oxidative stress - Abstract
Unbalanced nutrition early in life is increasingly recognized as an important factor in the development of chronic, non-communicable diseases at adulthood, including metabolic diseases. We aimed to determine whether transient postnatal overfeeding (OF) leads to liver stress-induced premature senescence (SIPS) of hepatocytes in association with liver structure and hepatic function alterations. Litters sizes of male C57BL/6 mice were adjusted to 9 pups (normal feeding, NF) or reduced to 3 pups during the lactation period to induce transient postnatal OF. Compared to the NF group, seven-month-old adult mice transiently overfed during the postnatal period were overweight and developed glucose intolerance and insulin resistance. Their livers showed microsteatosis and fibrosis, while hepatic insulin signaling and glucose transporter protein expressions were altered. Increased hepatic oxidative stress (OS) was observed, with increased superoxide anion production, glucose-6-phosphate dehydrogenase protein expression, oxidative DNA damage and decreased levels of antioxidant defense markers, such as superoxide dismutase and catalase proteins. Hepatocyte senescence was characterized by increased p21WAF, p53, Acp53, p16INK4a and decreased pRb/Rb and Sirtuin-1 (SIRT-1) protein expression levels. Transient postnatal OF induces liver OS at adulthood, associated with hepatocyte SIPS and alterations in liver structure and hepatic functions, which could be mediated by a SIRT-1 deficiency.
- Published
- 2016
42. Dépistage séquentiel de la FA silencieuse post-AVC (Stepwise screening for silent Atrial Fibrillation After Stroke : SAFAS study)
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Lucie Garnier, Yannick Béjot, Charles Guenancia, Alexandre Meloux, Mathilde Graber, and Catherine Vergely
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Gynecology ,medicine.medical_specialty ,Neurology ,business.industry ,medicine ,Atrial fibrillation ,Neurology (clinical) ,medicine.disease ,business - Abstract
Introduction Un tiers des AVC cryptogeniques seraient secondaires a une fibrillation atriale (FA) silencieuse non-detectee par les methodes usuelles. Trois versants seraient impliques dans le developpement d’une arythmie (le substrat atrial, le modulateur, le declencheur). Objectifs L’objectif etait d’identifier les deregulations physiopathologiques conduisant au developpement de la FA. Patients et methodes Etaient inclus les patients hospitalises pour un AVC ischemique au sein de l’USINV du CHU de Dijon, d’etiologie indeterminee a la prise en charge. Le depistage de la FA combinait de maniere sequentielle la telemetrie, le Holter ECG prolonge et le Holter sous cutane. Les donnees cliniques, echographiques, rythmiques et biologiques [dont les biomarqueurs tel que l’osteoprotegerine (OPG)] etaient comparees entre les patients en rythme sinusal (RS) et ceux developpant une FA, afin de determiner les predicteurs de FA. Resultats Sur les 40 patients analyses, 35 % presentaient une FA dont 50 % survenaient dans les 48 premieres heures. Les Holters longue duree detectaient 43 % de FA et 83 % de celles-ci survenaient au-dela des 24 h d’enregistrement habituelles. Le modele associant l’âge ≥ 75 ans, le volume indexe de l’oreillette gauche ≥ 26 mL/m2, le taux d’OPG ≥ 1190 pg/mL et le pNN50 (tonus parasympathique) sur le premier jour du scope permettait une excellente prediction de la survenue de la FA (AUC 0,897, p Discussion Ces resultats confirment la rentabilite d’un depistage precoce de la FA, notamment dans les 72 premieres heures. La dilatation de l’OG, marqueur de remodelage atrial a ete associee a la FA, paroxystique ou permanente, en post-AVC cryptogenique. Le systeme parasympathique jouent un role dans le declenchement de la FA et est aussi temoin de ce remodelage. Enfin, l’OPG, modulateur de l’inflammation, serait predictif de FA en regulant ce remodelage atrial. Conclusion Notre modele representant les 3 versants du developpement de l’arythmie etait predicteur de FA. Son depistage optimal et inedit, selon un schema sequentiel, prolonge et precoce limitait l’implantation de Holter ECG sous cutane. La poursuite des inclusions et des suivis est en cours.
- Published
- 2019
43. In patients with acute myocardial infarction, PCSK9 levels do not predict severity and recurrence of cardiovascular events
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Marianne Zeller, Catherine Vergely, Yves Cottin, Maud Maza, Luc Rochette, Gilles Lambert, and Michel Farnier
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Coronary angiography ,medicine.medical_specialty ,business.industry ,PCSK9 ,Disease ,University hospital ,medicine.disease ,Intensive care unit ,law.invention ,Coronary artery disease ,law ,Internal medicine ,medicine ,In patient ,Myocardial infarction ,Cardiology and Cardiovascular Medicine ,business - Abstract
Background In patients with coronary artery disease (CAD), it remains unclear whether serum PCSK9 levels can predict the severity of the disease and the risk of future cardiovascular events. Methods Among the patients admitted for an acute myocardial infarction (MI) from September 2015 to December 2016 in an intensive care unit from a university hospital, serum PCSK9 levels were measured on admission in patients not previously receiving statin therapy. We aimed to evaluate the association between PCSK9 levels, metabolic parameters, severity of CAD on coronary angiography, and the risk of in-hospital events and at one-year follow-up. Results In a total of 648 patients (mean age: 66 years, 67% male), the median PCSK9 was 263 ng/ml, higher for females compared with males (270 vs. 256 ng/mL, P 10 mg/L (P Conclusion In this large cohort of patients hospitalized for acute MI and not previously receiving statin therapy, PCSK9 levels do not predict the severity or the recurrence of cardiovascular events. The clinical utility of measuring PCSK9 levels remains to be demonstrated for this category of patients.
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- 2019
44. Nitric oxide synthase inhibition and oxidative stress in cardiovascular diseases: Possible therapeutic targets?
- Author
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Catherine Vergely, Marianne Zeller, Jean-Claude Guilland, Yves Cottin, Luc Lorgis, Julie Lorin, Luc Rochette, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Laboratoire de Physiopathologie et Pharmacologie Cardio-Métaboliques (U866, Lipides et nutrition, équipe 5) (LPPCM), Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), and Vergely, Catherine
- Subjects
NO inhibitors ,free radicals ,030204 cardiovascular system & hematology ,Protein degradation ,Pharmacology ,Nitric Oxide ,Nitric oxide ,03 medical and health sciences ,chemistry.chemical_compound ,BH 4 ,0302 clinical medicine ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,cardiovascular disease ,Enos ,medicine ,Animals ,Humans ,Pharmacology (medical) ,Enzyme Inhibitors ,Endothelial dysfunction ,Reactive nitrogen species ,030304 developmental biology ,NO synthases ,0303 health sciences ,biology ,Tetrahydrobiopterin ,biology.organism_classification ,medicine.disease ,[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,3. Good health ,ADMA ,Nitric oxide synthase ,Oxidative Stress ,chemistry ,Biochemistry ,Cardiovascular Diseases ,biology.protein ,Nitric Oxide Synthase ,Asymmetric dimethylarginine ,medicine.drug - Abstract
International audience; Nitric oxide (• NO) is synthetized enzymatically from L-arginine (L-Arg) by three NO synthase isoforms, iNOS, eNOS and nNOS. The synthesis of NO is selectively inhibited by guanidino-substituted analogs of L-Arg or methylarginines such as asymmetric dimethylarginine (ADMA), which results from protein degradation in cells. Many disease states, including cardiovascular diseases and diabetes, are associated with increased plasma levels of ADMA. The N-terminal catalytic domain of these NOS isoforms binds the heme prosthetic group as well as the redox cofactor, tetrahydrobiopterin (BH 4) associated with a regulatory protein, calmodulin (CaM). The enzymatic activity of NOS depends on substrate and cofactor availability. The importance of BH 4 as a critical regulator of eNOS function suggests that BH 4 may be a rational therapeutic target in vascular disease states. BH 4 oxidation appears to be a major contributor to vascular dysfunction associated with hypertension, ischemia/reperfusion injury, diabetes and other cardiovascular diseases as it leads to the increased formation of oxygen-derived radicals due to NOS uncoupling rather than NO. Accordingly, abnormalities in vascular NO production and transport result in endothelial dysfunction leading to various cardiovascular disorders. However, some disorders including a wide range of functions in the neuronal, immune and cardiovascular system were associated with the overproduction of NO. Inhibition of the enzyme should be a useful approach to treat these pathologies. Therefore, it appears that both a lack and excess of NO production in diseases can have various important pathological implications. In this context, NOS modulators (exogenous and endogenous) and their therapeutic effects are discussed.
- Published
- 2013
45. Postnatal Overfeeding in Rodents by Litter Size Reduction Induces Major Short- and Long-Term Pathophysiological Consequences
- Author
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Na Li, Catherine Vergely, Ahmed Habbout, and Luc Rochette
- Subjects
medicine.medical_specialty ,Litter Size ,media_common.quotation_subject ,Hypothalamus ,Appetite ,Medicine (miscellaneous) ,White adipose tissue ,Hyperphagia ,Biology ,Energy homeostasis ,Toxicology ,03 medical and health sciences ,chemistry.chemical_compound ,Overnutrition ,0302 clinical medicine ,Insulin resistance ,Corticosterone ,Internal medicine ,Brown adipose tissue ,medicine ,Animals ,Humans ,Hormone metabolism ,Obesity ,Infant Nutritional Physiological Phenomena ,030304 developmental biology ,media_common ,2. Zero hunger ,0303 health sciences ,Nutrition and Dietetics ,Leptin ,Infant ,medicine.disease ,Hormones ,Endocrinology ,medicine.anatomical_structure ,Adipose Tissue ,chemistry ,Cardiovascular Diseases ,Insulin Resistance ,Energy Intake ,030217 neurology & neurosurgery - Abstract
Numerous studies have demonstrated that the early postnatal environment can influence body weight and energy homeostasis into adulthood. Rodents raised in small litters have been shown to be a useful experimental model to study the short- and long-term consequences of early overnutrition, which can lead to modifications not only in body weight but also of several metabolic features. Postnatal overfeeding (PNOF) induces early malprogramming of the hypothalamic system, inducing acquired persisting central leptin and insulin resistance and an increase in orexigenic signals. Visceral white adipose tissue, lipogenic activity, and inflammatory status are increased in PNOF rodents, while brown adipose tissue shows reduced thermogenic activity. Pancreatic and hepatic glucose responsiveness is persistently reduced in PNOF rodents, which also frequently present disturbances in plasma lipids. PNOF rodents present increased circulating concentrations of leptin, elevated corticosterone secretion, and significant changes in glucocorticoid sensitivity. PNOF also influences nephrogenesis and renal maturation. Increased oxidative stress is also described in circulating blood and in some tissues, such as the heart or liver. At the cardiovascular level, a moderate increase in arterial blood pressure is sometimes observed and rapid cardiac hypertrophy is observed at weaning; however, during maturation, impaired contractility and fibrosis are observed. Myocardial genome expression is rapidly modified in overfed mice. Moreover, hearts of PNOF rodents are more sensitive to ischemia-reperfusion injury. Together, these results suggest that the nutritional state in the immediate postnatal period should be taken into account, because it may have an impact on cardiometabolic risk in adulthood.
- Published
- 2013
46. Short-term moderate diet restriction in adulthood can reverse oxidative, cardiovascular and metabolic alterations induced by postnatal overfeeding in mice
- Author
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Na Li, Lucie Desmoulins, Eve Rigal, Pauline Chollet, Luc Rochette, Olivier Hachet, Charles Guenancia, Catherine Vergely, Corinne Leloup, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre des Sciences du Goût et de l'Alimentation [Dijon] (CSGA), Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Lipides - Nutrition - Cancer (U866) ( LNC ), Université de Bourgogne ( UB ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon ( ENSBANA ), Service de Cardiologie [CHU de Dijon], Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ), Centre des Sciences du Goût et de l'Alimentation [Dijon] ( CSGA ), Institut National de la Recherche Agronomique ( INRA ) -Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique ( CNRS ), the French Ministry of Research, the Institut National de la Sante et de la Recherche Medicale (INSERM), the Regional Council of Burgundy and the Association de Cardiologie de Bourgogne (ACB)., Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Centre National de la Recherche Scientifique (CNRS)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB), université de Bourgogne, LNC, Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB)-Centre National de la Recherche Scientifique (CNRS), Vergely, Catherine, and Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique (CNRS)
- Subjects
Male ,0301 basic medicine ,Litter Size ,[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutrition ,Adipose tissue ,Mitochondria, Heart ,Mice ,0302 clinical medicine ,[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism ,Multidisciplinary ,Ejection fraction ,High-Fat Diet ,[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism ,[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism ,[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Adipose-Tissue ,coronary-heart-disease ,adipose-tissue ,insulin-resistance ,blood-pressure ,weight-gain ,rats ,obesity ,high-fat diet ,caloric restriction ,glucocorticoid metabolism ,Alimentation et Nutrition ,Blood-Pressure ,Body Composition ,medicine.symptom ,medicine.medical_specialty ,Respiratory rate ,030209 endocrinology & metabolism ,Oxidative phosphorylation ,Carbohydrate metabolism ,Biology ,Article ,03 medical and health sciences ,Insulin resistance ,Metabolic Diseases ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Internal medicine ,medicine ,Food and Nutrition ,Animals ,Obesity ,Glucocorticoid Metabolism ,Caloric Restriction ,Weight-Gain ,Insulin-Resistance ,Body Weight ,medicine.disease ,Rats ,Mice, Inbred C57BL ,[SDV.AEN] Life Sciences [q-bio]/Food and Nutrition ,Oxidative Stress ,030104 developmental biology ,Endocrinology ,Blood pressure ,Animals, Newborn ,Insulin Resistance ,Coronary-Heart-Disease ,[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition ,Weight gain - Abstract
We aimed to determine whether moderate diet restriction could restore cardiac, oxidative and metabolic alterations induced by postnatal overfeeding (PNOF). Litters of C57BL/6 male mice were either maintained at 9 (normal litter, NL), or reduced to 3 (small litter, SL) in order to induce PNOF. At 6 months, half of the NL and SL mice were subjected to 20% calorie-restriction (CR: NLCR, SLCR) for one month, while the other half continued to eat ad libitum (AL: NLAL, SLAL). Six-month old SL mice presented overweight, fat accumulation, hyperleptinemia, glucose intolerance, insulin resistance, increased cardiac ROS production and decreased left ventricular ejection fraction (LVEF). After CR, SL mice body weight was normalized; however, their fat mass and leptinemia were not decreased, glucose metabolism was improved and LVEF was increased. In SL mice, CR increased the cardiac mitochondrial respiratory rate and decreased cardiac ROS production. Hearts from SLCR mice showed better recovery and smaller postischemic infarct size. Intriguingly, no difference was observed between NLAL and NLCR mice for most of the parameters investigated. Short-term moderate CR not only normalized body weight in SL mice but also improved metabolic programming and reversed oxidative and cardiac dysfunction induced by PNOF.
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- 2016
47. Letter to the editor: 'Doxorubicin and ErbB2 overexpression: another piece in the mitochondrial jigsaw'
- Author
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Na Li, Catherine Vergely, Luc Rochette, Charles Guenancia, Physiopathologie et épidémiologie cérébro-cardiovasculaire [Dijon] (PEC2), and Université de Bourgogne (UB)-Université Bourgogne Franche-Comté [COMUE] (UBFC)
- Subjects
0301 basic medicine ,Cognitive science ,Focus (computing) ,Letter to the editor ,Physiology ,business.industry ,Receptor, ErbB-2 ,Jigsaw ,Mitochondria ,03 medical and health sciences ,030104 developmental biology ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Doxorubicin ,Physiology (medical) ,Medicine ,Signaling and Stress Response ,Cardiology and Cardiovascular Medicine ,business ,skin and connective tissue diseases ,neoplasms ,ComputingMilieux_MISCELLANEOUS - Abstract
This is the first study on ErbB2 overexpression in the heart that identifies cardioprotection after doxorubicin treatment. Our findings suggest that an adverse effect on redox signaling pathways necessary for maintaining mitochondrial antioxidant defenses may be an important mechanism of cardiac toxicity induced by drugs that target ErbB2 and Abl kinases.
- Published
- 2016
48. 0132 : Oxidative stress and cardio-metabolic alterations induced by postnatal programming can be reversed in adulthood by a short-term moderate caloric restriction
- Author
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Na Li, Charles Guenancia, Luc Rochette, Catherine Vergely, Corinne Leloup, Olivier Hachet, and Eve Rigal
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Cardiac function curve ,medicine.medical_specialty ,Ejection fraction ,biology ,business.industry ,Calorie restriction ,Carbohydrate metabolism ,medicine.disease_cause ,medicine.disease ,Insulin receptor ,Endocrinology ,Insulin resistance ,Internal medicine ,medicine ,biology.protein ,Weaning ,business ,Cardiology and Cardiovascular Medicine ,Oxidative stress - Abstract
Postnatal overfeeding (PNOF) in rodents induces early programming of cardio-metabolic risk. Our aim was to determine if a moderate diet restriction could restore cardio-metabolic alterations induced by PNOF. Immediately after birth, litters of C57BL/6 mice were either maintained at 9 (normal litter, NL), or reduced to 3 (small litter, SL) to induce PNOF. At weaning, all mice received a standard diet ad libitum (AL). At 6 month of age, half of the NL and SL mice were assigned to a moderate 20% calorie restriction (CR: NLCR, SLCR) for one month, while the other mice continued to eat AL (AL: NLAL, SLAL). Glucose and insulin tolerance tests, cardiac function (echocardiography), body composition (Echo-MRI), cardiac sensitivity to ischemia-reperfusion injury, mitochondrial function, reactive oxygen species (ROS) generation (EPR spectroscopy) and insulin signaling were assessed before and/or after one month of CR. Adult SL mice presented overweight, fat accumulation, hyperleptinemia, glucose intolerance, insulin resistance and decreased left ventricular ejection fraction (LVEF). After one month of moderate CR, body weight of SLCR was normalized to this of NLAL however their fat mass and leptinemia were not decreased. Glucose metabolism was improved and LVEF was increased In SLCR. After 30 min of global ischemia, hearts isolated from SLCR mice showed better recovery and smaller infarct size than this of others groups. CR increased the cardiac mitochondrial respiratory rate in SLCR mice whereas cardiac ROS production was significantly decreased in SLCR mice. Insulin signaling in heart was affected neither by PNOF nor by CR. Intriguingly, no difference was observed in NLCR mice for most of the parameters investigated. Our results confirmed the programming of early overfeeding on metabolic and cardiac function. A short-term moderate CR in not only normalized body weight in SL mice but also ameliorate the metabolic programming and reverse the cardiac dysfunction induced by PNOF. The author hereby declares no conflict of interest
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- 2016
- Full Text
- View/download PDF
49. Editorial
- Author
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Yves Cottin and Catherine Vergely-Vandriesse
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Cardiology and Cardiovascular Medicine - Published
- 2016
- Full Text
- View/download PDF
50. Editorial
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Yves Cottin and Catherine Vergely-Vandriesse
- Subjects
Cardiology and Cardiovascular Medicine - Published
- 2016
- Full Text
- View/download PDF
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