5 results on '"Laverny G"'
Search Results
2. Sarcopenia assessed by DXA and hand-grip dynamometer: a potential marker of damage, disability and myokines imbalance in inflammatory myopathies.
- Author
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Giannini M, Charles AL, Evrard C, Blaess J, Bouchard-Marmen M, Debrut L, Perniola S, Laverny G, Javier RM, Charloux A, Geny B, and Meyer A
- Subjects
- Humans, Female, Male, Middle Aged, Adult, Prospective Studies, Aged, Fibronectins blood, Case-Control Studies, Muscle, Skeletal diagnostic imaging, Muscle, Skeletal physiopathology, Biomarkers blood, Disability Evaluation, Myokines, Sarcopenia physiopathology, Sarcopenia blood, Sarcopenia diagnostic imaging, Sarcopenia etiology, Hand Strength physiology, Absorptiometry, Photon, Muscle Strength Dynamometer, Myositis physiopathology, Myositis blood
- Abstract
Objectives: To assess the ability of dual-energy X-ray absorptiometry (DXA) and hand-grip dynamometer to measure damage in inflammatory myopathies (IM)., Methods: Forty adult IM patients with a disease duration ≥12 months, low or no disease activity for ≥6 months, were prospectively enrolled. Thirty healthy age and sex-matched volunteers were enrolled as controls. Whole-body DXA and hand-grip dynamometer were used to measure muscle mass, grip strength and diagnose sarcopenia (EWGSOP2 criteria). Relationships between the results of strength in 12 muscles, functional tests, patient-reported disability, IMACS damage score, and history of the disease were assessed. The serum levels of potential molecular actors in the damage were measured., Results: DXA and grip strength measurements took ≤20 min. Both muscle mass and grip strength were decreased in IM patients vs volunteers (-10% and -30%, respectively) with a dispersion that varied widely (interquartile range -24.3% to +7.8% and -51.3% to -18.9%, respectively). Muscle mass and grip strength were non-redundantly correlated (r up to 0.6, P = 0.0001) with strength in 14 muscles (manual muscle test and hand-held dynamometer), functions (of limbs, respiratory and deglutition muscles), patient-reported disability, damage (extension and severity in muscular and extra-muscular domains) and blood levels of several myokines. Seven IM patients (17.5%) were sarcopenic. They had the worst damage, impaired functions, disability and history of severe myopathy. Decreased irisin and osteonectin levels were associated with sarcopenia (area under the curve 0.71 and 0.80, respectively)., Conclusion: DXA and hand-grip dynamometer are useful tools to assess damage in IM. Irisin and osteonectin may play a role in IM damage pathogenesis., (© The Author(s) 2024. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please email: journals.permissions@oup.com.)
- Published
- 2024
- Full Text
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3. 4-Hydroxy-1α,25-Dihydroxyvitamin D 3 : Synthesis and Structure-Function Study.
- Author
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Peluso-Iltis C, Pierrat N, Rovito D, Osz J, Sawada D, Kittaka A, Laverny G, and Rochel N
- Subjects
- Animals, Mice, Structure-Activity Relationship, Rats, Calcitriol analogs & derivatives, Calcitriol chemistry, Calcitriol metabolism, Calcitriol chemical synthesis, Male, Vitamin D analogs & derivatives, Vitamin D metabolism, Vitamin D chemistry, Hypercalcemia metabolism, Kidney metabolism, Receptors, Calcitriol metabolism, Receptors, Calcitriol chemistry, Receptors, Calcitriol genetics
- Abstract
The active vitamin D metabolites, 25-hydroxyvitamin D
3 (25D3 ) and 1,25-dihydroxyvitamin D3 (1,25D3 ), are produced by successive hydroxylation steps and play key roles in several cellular processes. However, alternative metabolic pathways exist, and among them, the 4-hydroxylation of 25D3 is a major one. This study aims to investigate the structure-activity relationships of 4-hydroxy derivatives of 1,25D3 . Structural analysis indicates that 1,4α,25(OH)3 D3 and 1,4β,25(OH)3 D3 maintain the anchoring hydrogen bonds of 1,25D3 and form additional interactions, stabilizing the active conformation of VDR. In addition, 1,4α,25D3 and 1,4β,25D3 are as potent as 1,25D3 in regulating the expression of VDR target genes in rat intestinal epithelial cells and in the mouse kidney. Moreover, these two 4-hydroxy derivatives promote hypercalcemia in mice at a dose similar to that of the parent compound.- Published
- 2024
- Full Text
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4. LSD1 inhibition circumvents glucocorticoid-induced muscle wasting of male mice.
- Author
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Cai Q, Sahu R, Ueberschlag-Pitiot V, Souali-Crespo S, Charvet C, Silem I, Cottard F, Ye T, Taleb F, Metzger E, Schuele R, Billas IML, Laverny G, Metzger D, and Duteil D
- Subjects
- Animals, Male, Mice, Mice, Inbred C57BL, Gene Expression Regulation drug effects, Histone Demethylases metabolism, Histone Demethylases antagonists & inhibitors, Histone Demethylases genetics, Glucocorticoids pharmacology, Dexamethasone pharmacology, Receptors, Glucocorticoid metabolism, Muscular Atrophy chemically induced, Muscular Atrophy metabolism, Muscular Atrophy pathology, Muscular Atrophy drug therapy, Muscle, Skeletal metabolism, Muscle, Skeletal drug effects, Muscle, Skeletal pathology
- Abstract
Synthetic glucocorticoids (GC), such as dexamethasone, are extensively used to treat chronic inflammation and autoimmune disorders. However, long-term treatments are limited by various side effects, including muscle atrophy. GC activities are mediated by the glucocorticoid receptor (GR), that regulates target gene expression in various tissues in association with cell-specific co-regulators. Here we show that GR and the lysine-specific demethylase 1 (LSD1) interact in myofibers of male mice, and that LSD1 connects GR-bound enhancers with NRF1-associated promoters to stimulate target gene expression. In addition, we unravel that LSD1 demethylase activity is required for triggering starvation- and dexamethasone-induced skeletal muscle proteolysis in collaboration with GR. Importantly, inhibition of LSD1 circumvents muscle wasting induced by pharmacological levels of dexamethasone, without affecting their anti-inflammatory activities. Thus, our findings provide mechanistic insights into the muscle-specific GC activities, and highlight the therapeutic potential of targeting GR co-regulators to limit corticotherapy-induced side effects., (© 2024. The Author(s).)
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- 2024
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5. Targeting Mitochondrial Dynamics during Lower-Limb Ischemia Reperfusion in Young and Old Mice: Effect of Mitochondrial Fission Inhibitor-1 (mDivi-1).
- Author
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Paradis S, Charles AL, Giannini M, Meyer A, Lejay A, Talha S, Laverny G, Charloux A, and Geny B
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- Humans, Animals, Mice, Aged, Mitochondrial Dynamics, Calcium, Ischemia drug therapy, Muscle, Skeletal, Lactic Acid, Superoxide Dismutase, Peripheral Arterial Disease, Mitochondrial Diseases, Quinazolinones
- Abstract
Peripheral arterial disease (PAD) strikes more than 200 million people worldwide and has a severe prognosis by potentially leading to limb amputation and/or death, particularly in older patients. Skeletal muscle mitochondrial dysfunctions and oxidative stress play major roles in this disease in relation with ischemia-reperfusion (IR) cycles. Mitochondrial dynamics through impairment of fission-fusion balance may contribute to skeletal muscle pathophysiology, but no data were reported in the setting of lower-limb IR despite the need for new therapeutic options. We, therefore, investigated the potential protective effect of mitochondrial division inhibitor-1 (mDivi-1; 50 mg/kg) in young (23 weeks) and old (83 weeks) mice submitted to two-hour ischemia followed by two-hour reperfusion on systemic lactate, muscle mitochondrial respiration and calcium retention capacity, and on transcripts specific for oxidative stress and mitochondrial dynamics. At the systemic levels, an IR-related increase in circulating lactate was still major despite mDivi-1 use (+305.9% p < 0.0001, and +269.4% p < 0.0001 in young and old mice, respectively). Further, IR-induced skeletal muscle mitochondrial dysfunctions (more severely impaired mitochondrial respiration in old mice (OXPHOS CI state, -68.2% p < 0.0001 and -84.9% p < 0.0001 in 23- and 83-week mice) and reduced calcium retention capacity (-46.1% p < 0.001 and -48.2% p = 0.09, respectively) were not corrected by mDivi-1 preconditioning, whatever the age. Further, mDivi-1 treatment did not oppose superoxide anion production (+71.4% p < 0.0001 and +37.5% p < 0.05, respectively). At the transcript level, markers of antioxidant enzymes (SOD 1, SOD 2, catalase, and GPx) and fission markers (Drp1, Fis) remained unchanged or tended to be decreased in the ischemic leg. Fusion markers such as mitofusin 1 or 2 decreased significantly after IR in both groups. In conclusion, aging enhanced the deleterious effects or IR on muscle mitochondrial respiration, and in this setting of lower-limb IR, mDivi-1 failed to protect the skeletal muscle both in young and old mice.
- Published
- 2024
- Full Text
- View/download PDF
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