104 results on '"Crola Da Silva, C."'
Search Results
2. The influence of early post-STEMI inflammation on diastolic function: diagnostic and therapeutic implications
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Filip, S, primary, Leboube, S, additional, Thibault, H, additional, Bergerot, C, additional, Paccalaet, A, additional, Hayek, A, additional, Rioufol, G, additional, Bonnefoy-Cudraz, E, additional, Prieur, C, additional, Crola Da Silva, C, additional, Brun, C, additional, Mewton, N, additional, Mechtouff, L, additional, and Bochaton, T, additional
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- 2023
- Full Text
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3. Inhibition of myocardial reperfusion injury by ischemic postconditioning requires sirtuin 3-mediated deacetylation of cyclophilin D
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Bochaton, T., Crola-Da-Silva, C., Pillot, B., Villedieu, C., Ferreras, L., Alam, M.R., Thibault, H., Strina, M., Gharib, A., Ovize, M., and Baetz, D.
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- 2015
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4. Inflammatory profile and white matter hyperintensity burden in acute ischemic stroke patients
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Rascle, L., Nighoghossian, N., Cho, T. H., Bochaton, T., Paccalet, A., Crola da Silva, C., Buisson, Marielle, Amaz, C., Fontaine, J., Ong, E., Derex, L., Berthezene, Y., Eker, O. F., Mewton, N., Ovize, M., Mechtouff, L., Hospices Civils de Lyon (HCL), Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Centre d'Investigation Clinique [Bron] (CIC1407), Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Groupement Hospitalier Est [Bron], Hôpital neurologique et neurochirurgical Pierre Wertheimer [CHU - HCL], Centre de Recherche en Acquisition et Traitement de l'Image pour la Santé (CREATIS), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and CarMeN, laboratoire
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Inflammation ,[SDV]Life Sciences [q-bio] ,Immunology ,Cerebral small vessel diseases ,Magnetic Resonance Imaging ,White Matter ,Blood biomarkers ,Brain Ischemia ,Reperfusion injury ,[SDV] Life Sciences [q-bio] ,Stroke ,Neurology ,Immunology and Allergy ,Humans ,Neurology (clinical) ,Biomarkers ,Thrombectomy ,Ischemic Stroke - Abstract
International audience; Inflammation is involved in small vessel disease (SVD). We aim to clarify whether inflammation related to white matter hyperintensities (WMH), a key component of SVD, may affect the inflammatory response in acute ischemic stroke (AIS) patients. For this, we sequentially measured 10 circulating inflammatory markers and assessed WMH burden on admission MRI in AIS patients treated with thrombectomy. Of 149 patients, 57 (38.3%) had a high WMH burden (Fazekas≥3). A high WMH burden was associated with 4 markers levels but this association did not remain following multivariable analyses. WMH burden is not associated with a specific inflammatory profile in AIS.
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- 2022
5. Base des phénomènes d’ischémie reperfusion et de la protection myocardique
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Benhabbouche, S., Crola da silva, C., Abrial, M., and Ferrera, R.
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- 2011
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6. Myocardial ischemia-reperfusion and diabetes: The crux of animal model choice
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Dia, M., primary, Paccalet, A., additional, Pillot, B., additional, Leon, C., additional, Ovize, M., additional, Crola Da Silva, C., additional, Bochaton, T., additional, and Paillard, M., additional
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- 2021
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7. Development of multiparametric analysis of human PBMC by flow cytometry: Determination of inflammatory and calcic profile
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Brun, C., primary, Paccalet, A., additional, Bochaton, T., additional, Paillard, M., additional, and Crola Da Silva, C., additional
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- 2021
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8. Leptin serum level is associated with clinical outcome after STEMI
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Paccalet, A., primary, Crola Da Silva, C., additional, Leboube, S., additional, Mechtouff, L., additional, Paillard, M., additional, Amaz, C., additional, Varillon, Y., additional, De Bourguignon, C., additional, Cartier, Y., additional, Prieur, C., additional, Hayek, A., additional, Derimay, F., additional, Rioufol, G., additional, Bonnefoy, C., additional, Mewton, N., additional, Ovize, M., additional, Bidaux, G., additional, and Bochaton, T., additional
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- 2021
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9. Matrix Metalloproteinase-9 Relationship With Infarct Growth and Hemorrhagic Transformation in the Era of Thrombectomy
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Mechtouff, L., Bochaton, T., Paccalet, A., Crola Da Silva, C., Buisson, M., Amaz, C., Bouin, M., Derex, L., Ong, E., Berthezene, Y., Eker, O. F., Dufay, N., Mewton, N., Ovize, M., Nighoghossian, N., Cho, T. H., Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Hôpital neurologique et neurochirurgical Pierre Wertheimer [CHU - HCL], Hospices Civils de Lyon (HCL), Centre d'Investigation Clinique [Bron] (CIC1407), Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Groupement Hospitalier Est [Bron], Hôpital Louis Pradel [CHU - HCL], Centre de Recherche en Acquisition et Traitement de l'Image pour la Santé (CREATIS), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Modeling & analysis for medical imaging and Diagnosis (MYRIAD), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Centre de Recherche et d'Application en Traitement de l'Image et du Signal (CREATIS), Université de Lyon-Université de Lyon-École Supérieure de Chimie Physique Électronique de Lyon (CPE)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Department of Cardiology, Imagerie Tomographique et Radiothérapie, CarMeN, laboratoire, Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hospices Civils de Lyon (HCL), Imagerie et modélisation Vasculaires, Thoraciques et Cérébrales (MOTIVATE), Université Jean Monnet [Saint-Étienne] (UJM)-Hospices Civils de Lyon (HCL)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Jean Monnet [Saint-Étienne] (UJM)-Hospices Civils de Lyon (HCL)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-École Supérieure Chimie Physique Électronique de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)
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Neurology ,thrombectomy ,[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology ,[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology ,matrix metalloproteinase 9 ,Neurology (clinical) ,stroke ,Original Research ,MRI ,thrombolytic therapy - Abstract
International audience; Objective: To assess the relationship between matrix metalloproteinase 9 (MMP-9), a proteolytic enzyme involved in the breakdown of the blood-brain barrier, and infarct growth and hemorrhagic transformation in acute ischemic stroke (AIS) with large vessel occlusion (LVO) in the era of mechanical thrombectomy (MT) using the kinetics of MMP-9 and sequential magnetic resonance imaging (MRI).Methods: HIBISCUS-STROKE is a cohort study including AIS patients with LVO treated with MT following admission MRI. Patients underwent sequential assessment of MMP-9, follow-up CT at day 1, and MRI at day 6. The CT scan at day 1 classified any hemorrhagic transformation according to the European Co-operative Acute Stroke Study-II (ECASS II) classification. Infarct growth was defined as the difference between final Fluid-Attenuated Inversion Recovery volume and baseline diffusion-weighted imaging volume. Conditional logistic regression analyses were adjusted for main confounding variables including reperfusion status.Results: One hundred and forty-eight patients represent the study population. A high MMP-9 level at 6 h from admission (H6) (p = 0.02), a high glucose level (p = 0.01), a high temperature (p = 0.04), and lack of reperfusion (p = 0.02) were associated with infarct growth. A high MMP-9 level at H6 (p = 0.03), a high glucose level (p = 0.03) and a long delay from symptom onset to groin puncture (p = 0.01) were associated with hemorrhagic transformation.Conclusions: In this MT cohort study, MMP-9 level at H6 predicts infarct growth and hemorrhagic transformation.
- Published
- 2020
10. IL-10 / IL-6 serum ratio as a prognosis marker of STEMI
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Leboube, S, primary, Bochaton, T, additional, Paccalet, A, additional, Crola Da Silva, C, additional, Jeantet, P, additional, Amaz, C, additional, De Bourguignon, C, additional, Varillon, Y, additional, Prieur, C, additional, Tomasevic, D, additional, Genot, N, additional, Rioufol, G, additional, Bonnefoy-Cudraz, E, additional, Mewton, N, additional, and Ovize, M, additional
- Published
- 2020
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11. Basophil count as a prognosis biomarker after STEMI
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Charbonnieras, F., primary, Bochaton, T., additional, Paccalet, A., additional, Jeantet, P., additional, Crola Da Silva, C., additional, Amaz, C., additional, De Bourguignon, C., additional, Prieur, C., additional, Tomasevic, D., additional, Genot, N., additional, Rioufol, G., additional, Bonnefoy-Cudraz, E., additional, Mewton, N., additional, and Ovize, M., additional
- Published
- 2020
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12. IL-10/IL-6 serum ratio as a prognosis marker of STEMI
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Leboube, S., primary, Bochaton, T., additional, Paccalet, A., additional, Crola Da Silva, C., additional, Jeantet, P., additional, Amaz, C., additional, De Bourguignon, C., additional, Varillon, Y., additional, Prieur, C., additional, Tomasevic, D., additional, Genot, N., additional, Rioufol, G., additional, Bonnefoy-Cudraz, E., additional, Mewton, N., additional, and Ovize, M., additional
- Published
- 2020
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13. An innovative sequence of hypoxia-reoxygenation on adult mouse cardiomyocytes in suspension to perform multilabeling analysis by flow cytometry
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Tessier, N., primary, Paccalet, A., additional, Paillard, M., additional, Paita, L., additional, Gomez, L., additional, Gallo-Bona, N., additional, Chouabe, C., additional, Leon, C., additional, Badawi, S., additional, Harhous, Z., additional, Ovize, M., additional, and Crola Da Silva, C., additional
- Published
- 2020
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14. Serum soluble tumor necrosis factor receptor (sTNFR) 1 and 2 in STEMI
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Paccalet, A., primary, Bochaton, T., additional, Jantet, P., additional, Cartier, R., additional, Prieur, C., additional, Amaz, C., additional, Jossan, C., additional, Rioufol, G., additional, Leboube, S., additional, Crola Da Silva, C., additional, Mewton, N., additional, and Ovize, M., additional
- Published
- 2020
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15. Association of myocardial edema, hemorrhage and persistent microvascular obstruction with circulating inflammatory biomarkers in acute myocardial infarction patient
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Paccalet, A., primary, Bochaton, T., additional, Lassus, J., additional, Derimay, F., additional, Rioufol, G., additional, Prieur, C., additional, Bonnefoy-Cudraz, E., additional, Crola Da Silva, C., additional, Amaz, C., additional, Jossan, C., additional, Monneret, G., additional, Ovize, M., additional, and Mewton, N., additional
- Published
- 2019
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16. TRPV1 inhibition supports cell survival during hypoxia/reoxygenation in the rat cardiomyoblast H9C2 cell line
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Tessier, N., primary, Chouabe, C., additional, Crola Da Silva, C., additional, Ovize, M., additional, Van Coppenolle, F., additional, and Ducreux, S., additional
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- 2019
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17. Inflammatory biomarkers kinetic in STEMI patients and their relationship with infarct size and LVEF
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Bochaton, T., primary, Paccalet, A., additional, Crola Da Silva, C., additional, Baetz, D., additional, Genot, N., additional, Prieur, C., additional, Tomasevic, D., additional, Jossan, C., additional, Amaz, C., additional, Dufay, N., additional, Bonnefoy-Cudraz, E., additional, Mewton, N., additional, and Ovize, M., additional
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- 2019
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18. P1681Daytime variation of infarct size in STEMI patients
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Bochaton, T, primary, Bernelin, H, additional, Paccalet, A, additional, Crola Da Silva, C, additional, Baetz, D, additional, Genot, N, additional, Prieur, C, additional, Tomasevic, D, additional, Jossan, C, additional, Amaz, C, additional, Dufay, N, additional, Rioufol, G, additional, Bonnefoy-Cudraz, E, additional, Mewton, N, additional, and Ovize, M, additional
- Published
- 2018
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19. Circadian variations of infarct size and inflammation response in patients presenting a STEMI
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Bochaton, T., primary, Bernelin, H., additional, Paccalet, A., additional, Crola Da Silva, C., additional, Baetz, D., additional, Bonnefoy-Cudraz, E., additional, Mewton, N., additional, and Ovize, M., additional
- Published
- 2018
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20. Heart clearing opens new insights in the quantification of injured area after ischemia reperfusion
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Paccalet, A., primary, Badawi, S., additional, Gouriou, Y., additional, Bidaux, G., additional, and Crola Da Silva, C., additional
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- 2018
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21. What are the effects of the guidelines-recommended treatments of myocardial infarction on the secretion of pro- and anti-inflammatory cytokins in an in vitro murin inflammatory model?
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Plaine, B., primary, Bochaton, T., additional, Paccalet, A., additional, Crola-Da-Silva, C., additional, Bonnefoy-Cudraz, E., additional, Mewton, N., additional, and Ovize, M., additional
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- 2018
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22. Endothelial activation and infarct size at the acute phase of myocardial infarction
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Falque, H., primary, Bochaton, T., additional, Bernelin, H., additional, Paccalet, A., additional, Crola Da Silva, C., additional, Baetz, D., additional, Bonnefoy-Cudraz, E., additional, Mewton, N., additional, and Ovize, M., additional
- Published
- 2018
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23. Cardioprotective role of Transient Receptor Potential Vanilloid 1 (TRPV1) channels in H9C2 cell line
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Tessier, N., primary, Chouabe, C., additional, Crola Da Silva, C., additional, Bonvallet, R., additional, Ovize, M., additional, Ducreux, S., additional, and Van Coppenolle, F., additional
- Published
- 2018
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24. Protection of Human Pancreatic Islets from Lipotoxicity by Modulation of the Translocon
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Cassel, R., primary, Ducreux, S., additional, Alam, M. R., additional, Dingreville, F., additional, Berlé, C., additional, Burda-Jacob, K., additional, Chauvin, M. A., additional, Chikh, K., additional, Païta, L., additional, Al-Mawla, R., additional, Crola Da Silva, C., additional, Rieusset, J., additional, Thivolet, C., additional, Van Coppenolle, F., additional, and Madec, A. M., additional
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- 2016
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25. Erratum: The SR/ER-mitochondria calcium crosstalk is regulated by GSK3β during reperfusion injury
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Gomez, L, primary, Thiebaut, P-A, additional, Paillard, M, additional, Ducreux, S, additional, Abrial, M, additional, Crola Da Silva, C, additional, Durand, A, additional, Alam, M R, additional, Van Coppenolle, F, additional, Sheu, S-S, additional, and Ovize, M, additional
- Published
- 2015
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26. The SR/ER-mitochondria calcium crosstalk is regulated by GSK3β during reperfusion injury
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Gomez, L, primary, Thiebaut, P-A, additional, Paillard, M, additional, Ducreux, S, additional, Abrial, M, additional, Crola Da Silva, C, additional, Durand, A, additional, Alam, M R, additional, Van Coppenolle, F, additional, Sheu, S-S, additional, and Ovize, M, additional
- Published
- 2015
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27. The SR/ER-mitochondria calcium crosstalk is regulated by GSK3β during reperfusion injury
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Gomez, L, Thiebaut, P-A, Paillard, M, Ducreux, S, Abrial, M, Crola Da Silva, C, Durand, A, Alam, M R, Van Coppenolle, F, Sheu, S-S, and Ovize, M
- Abstract
Glycogen synthase kinase-3β (GSK3β) is a multifunctional kinase whose inhibition is known to limit myocardial ischemia–reperfusion injury. However, the mechanism mediating this beneficial effect still remains unclear. Mitochondria and sarco/endoplasmic reticulum (SR/ER) are key players in cell death signaling. Their involvement in myocardial ischemia–reperfusion injury has gained recognition recently, but the underlying mechanisms are not yet well understood. We questioned here whether GSK3β might have a role in the Ca2+transfer from SR/ER to mitochondria at reperfusion. We showed that a fraction of GSK3β protein is localized to the SR/ER and mitochondria-associated ER membranes (MAMs) in the heart, and that GSK3β specifically interacted with the inositol 1,4,5-trisphosphate receptors (IP3Rs) Ca2+channeling complex in MAMs. We demonstrated that both pharmacological and genetic inhibition of GSK3β decreased protein interaction of IP3R with the Ca2+channeling complex, impaired SR/ER Ca2+release and reduced the histamine-stimulated Ca2+exchange between SR/ER and mitochondria in cardiomyocytes. During hypoxia reoxygenation, cell death is associated with an increase of GSK3β activity and IP3R phosphorylation, which leads to enhanced transfer of Ca2+from SR/ER to mitochondria. Inhibition of GSK3β at reperfusion reduced both IP3R phosphorylation and SR/ER Ca2+release, which consequently diminished both cytosolic and mitochondrial Ca2+concentrations, as well as sensitivity to apoptosis. We conclude that inhibition of GSK3β at reperfusion diminishes Ca2+leak from IP3R at MAMs in the heart, which limits both cytosolic and mitochondrial Ca2+overload and subsequent cell death.
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- 2016
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28. Kinetics and Prognosis Value of CCL5/RANTES at the Acute Phase of ST-Segment-Elevation Myocardial Infarction.
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Brun C, Moulin F, Leboube S, Hayek A, Kaczmarczyk A, Saleh IA, Prieur C, Varillon Y, Bonnefoy-Cudraz E, Mewton NO, Bidaux G, Crola Da Silva C, Paillard M, Ducreux S, and Bochaton T
- Subjects
- Humans, Male, Female, Middle Aged, Prospective Studies, Aged, Prognosis, Time Factors, Severity of Illness Index, Enzyme-Linked Immunosorbent Assay, Predictive Value of Tests, Kinetics, Chemokine CCL5 blood, ST Elevation Myocardial Infarction blood, ST Elevation Myocardial Infarction diagnosis, ST Elevation Myocardial Infarction surgery, Biomarkers blood, Percutaneous Coronary Intervention
- Abstract
Background: RANTES (regulated upon activation, normal T cell expressed, and secreted) or CCL5 (CC chemokine ligand 5) is a chemokine that mediates chemotaxis and activation of T cells, monocytes, mast cells, and dendritic cells. It is involved in the pathogenesis of several diseases, including atherosclerosis, but its role at the acute phase of myocardial infarction (MI) is unclear. Our objective is to determine whether the serum level of RANTES is a marker of the severity of acute MI., Methods and Results: The study included 250 consecutive patients with ST-segment-elevation MI who underwent percutaneous coronary intervention in a prospective cohort. Peripheral venous blood samples were taken at 5 time points and ELISA was performed. Major adverse cardiovascular events were prospectively recorded over the 12-month follow-up. Serum RANTES level raised from 12.9 (8.0-20.7) ng/mL at H0 to 13.9 (7.4-22.4) ng/mL at H4 and decreased gradually until 1 month at 9.7 (5.4-13.6) ng/mL ( P <0.0001). RANTES area under the curve (AUC) level was not correlated with infarct size ( r =-0.03, P =0.70) or left ventricular ejection fraction assessed by magnetic resonance imaging ( r =0.02, P =0.80). Patients with a RANTES AUC serum level below the first tertile value of the population (411.0 ng.h.mL
-1 ) were more likely to have a major adverse cardiovascular event during the first 12 months after ST-segment-elevation MI (hazard ratio [HR], 2.9 [1.3-6.6], P =0.01). In a multivariable Cox regression analysis, serum level below the first tertile remained associated with an increased risk of experiencing major adverse cardiovascular event during the follow-up (adjusted HR, 2.6 [1.2-5.8], P =0.02)., Conclusions: A low level of circulating RANTES post ST-segment-elevation MI was associated with an increased risk of experiencing major adverse cardiovascular event and might be a valuable prognostic marker in patients with ST-segment-elevation MI.- Published
- 2024
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29. SEMA3A as a biomarker of primary ventricular fibrillation complicating STEMI.
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Boiteux C, Leboube S, Hayek A, Brun C, Bessiere F, Mewton N, Bidaux G, Crola Da Silva C, Chevalier P, and Bochaton T
- Abstract
Competing Interests: Disclosures The authors have no conflicts of interest to disclose.
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- 2024
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30. Soluble Programmed Death-1 Predicts Clinical Outcome After STEMI.
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Hayek A, Brun C, Leboube S, Moulin F, Mewton N, Bidaux G, Ducreux S, Paillard M, Crola Da Silva C, and Bochaton T
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- 2024
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31. Deleterious Anti-Inflammatory Macrophage Recruitment in Early Post-Infarction Phase: Unraveling the IL-6/MCP-1/STAT3 Axis.
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Paccalet A, Badawi S, Pillot B, Augeul L, Mechtouff L, Harhous Z, Gouriou Y, Paillard M, Breuilly M, Amaz C, Varillon Y, Leboube S, Brun C, Prieur C, Rioufol G, Mewton N, Ovize M, Bidaux G, Bochaton T, and Crola Da Silva C
- Abstract
Using a translational approach with an ST-segment myocardial infarction (STEMI) cohort and mouse model of myocardial infarction, we highlighted the role of the secreted IL-6 and MCP-1 cytokines and the STAT3 pathway in heart macrophage recruitment and activation. Cardiac myocytes secrete IL-6 and MCP-1 in response to hypoxic stress, leading to a recruitment and/or polarization of anti-inflammatory macrophages via the STAT3 pathway. In our preclinical model of myocardial infarction, neutralization of IL-6 and MCP-1 or STAT3 pathway reduced infarct size. Together, our data demonstrate that anti-inflammatory macrophages can be deleterious in the acute phase of STEMI., Competing Interests: This work was supported by “Federation Française de Cardiologie,” and LABEX CORTEX (ANR-11-LABX-0042) and FRM (FD202012010540). The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2024 The Authors.)
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- 2024
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32. A bibliometric analysis: Ca 2+ fluxes and inflammatory phenotyping by flow cytometry in peripheral blood mononuclear cells.
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Brun C, Chalet L, Moulin F, Bochaton T, Ducreux S, Paillard M, and Crola Da Silva C
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- Humans, Flow Cytometry methods, Cell Line, Inflammation metabolism, Leukocytes, Mononuclear metabolism, Signal Transduction
- Abstract
Background: The immune system, composed of organs, tissues, cells, and proteins, is the key to protecting the body from external biological attacks and inflammation. The latter occurs in several pathologies, such as cancers, type 1 diabetes, and human immunodeficiency virus infection. Immunophenotyping by flow cytometry is the method of choice for diagnosing these pathologies. Under inflammatory conditions, the peripheral blood mononuclear cells (PBMCs) are partially activated and generate intracellular pathways involving Ca
2+ -dependent signaling cascades leading to transcription factor expression. Ca2+ signaling is typically studied by microscopy in cell lines but can present some limitations to explore human PBMCs, where flow cytometry can be a good alternative., Objective: In this review, we dived into the research field of inflammation and Ca2+ signaling in PBMCs. We aimed to investigate the structure and evolution of this field in a physio-pathological context, and then we focused our review on flow cytometry analysis of Ca2+ fluxes in PBMCs., Methods: From 1984 to 2022, 3865 articles on inflammation and Ca2+ signaling in PBMCs were published, according to The Clarivate Web of Science (WOS) database used in this review. A bibliometric study was designed for this collection and consisted of a co-citation and bibliographic coupling analysis., Results: The co-citation analysis was performed on 133 articles: 4 clusters highlighted the global context of Ca2+ homeostasis, including chemical probe development, identification of the leading players in Ca2+ signaling, and the link with chemokine production in immune cell function. Next, the bibliographic coupling analysis combined 998 articles in 8 clusters. This analysis outlined the mechanisms of PBMC activation, from signal integration to cellular response. Further explorations of the bibliographic coupling network, focusing on flow cytometry, revealed 21 articles measuring cytosolic Ca2+ in PBMCs, with only 5 since 2016. This final query showed that Ca2+ signaling analysis in human PBMCs using flow cytometry is still underdeveloped and investigates mainly the cytosolic Ca2+ compartment., Conclusion: Our review uncovers remaining knowledge gaps of intracellular players involved in Ca2+ signaling in PBMCs, such as reticulum and mitochondria, and presents flow cytometry as a solid option to supplement gold-standard microscopy studies., Competing Interests: LC was employed by Olea Medical. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Brun, Chalet, Moulin, Bochaton, Ducreux, Paillard and Crola Da Silva.)- Published
- 2023
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33. TRPV1 Channels Are New Players in the Reticulum-Mitochondria Ca 2+ Coupling in a Rat Cardiomyoblast Cell Line.
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Tessier N, Ducrozet M, Dia M, Badawi S, Chouabe C, Crola Da Silva C, Ovize M, Bidaux G, Van Coppenolle F, and Ducreux S
- Subjects
- Animals, Rats, Mitochondria, Endoplasmic Reticulum, Cell Line, Endoplasmic Reticulum Stress, Transient Receptor Potential Channels, Antineoplastic Agents
- Abstract
The Ca
2+ release in microdomains formed by intercompartmental contacts, such as mitochondria-associated endoplasmic reticulum membranes (MAMs), encodes a signal that contributes to Ca2+ homeostasis and cell fate control. However, the composition and function of MAMs remain to be fully defined. Here, we focused on the transient receptor potential vanilloid 1 (TRPV1), a Ca2+ -permeable ion channel and a polymodal nociceptor. We found TRPV1 channels in the reticular membrane, including some at MAMs, in a rat cardiomyoblast cell line (SV40-transformed H9c2) by Western blotting, immunostaining, cell fractionation, and proximity ligation assay. We used chemical and genetic probes to perform Ca2+ imaging in four cellular compartments: the endoplasmic reticulum (ER), cytoplasm, mitochondrial matrix, and mitochondrial surface. Our results showed that the ER Ca2+ released through TRPV1 channels is detected at the mitochondrial outer membrane and transferred to the mitochondria. Finally, we observed that prolonged TRPV1 modulation for 30 min alters the intracellular Ca2+ equilibrium and influences the MAM structure or the hypoxia/reoxygenation-induced cell death. Thus, our study provides the first evidence that TRPV1 channels contribute to MAM Ca2+ exchanges.- Published
- 2023
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34. Specific inflammatory profile of acute ischemic stroke patients with left atrial enlargement.
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Fontaine J, Leboube S, Bochaton T, Thibault H, Amaz C, Cho TH, Paccalet A, Crola Da Silva C, Duhamel S, Buisson M, Rascle L, Bidaux G, Ovize M, Nighoghossian N, and Mechtouff L
- Abstract
Background: The inflammatory process underlying atrial myopathy may affect the inflammatory response activated in acute ischemic stroke (AIS)., Objectives: We aimed to assess whether left atrial enlargement (LAE) as a marker of atrial myopathy is associated with a different profile of circulating inflammatory markers in AIS patients., Methods: HIBISCUS-STROKE is a cohort study including anterior circulation AIS patients treated with mechanical thrombectomy following MRI. Ten circulating inflammatory markers were measured at admission and 6, 24, and 48 h after admission. LAE was defined as a left atrial volume index (LAVi) ≥34 ml/m
2 . A multiple logistic regression model was performed to detect an independent association between the area under the curve (AUC) of these markers and LAE., Results: We included 143 patients. Of them, 85 (59.4%) had LAE. On univariable analysis, we found that patients with LAE had higher soluble form suppression of tumorigenicity 2 (sST2), soluble tumor necrosis factor receptor I (sTNFR1), and vascular cellular adhesion molecule-1 (VCAM-1) AUC, were older, mostly female, had a higher National Institutes of Health Stroke Scale (NIHSS) score and blood glucose level at admission, had more often hypertension, and a cardioembolic source of AIS, such as atrial fibrillation, while they were less frequently current smokers and had a lower rate of tandem occlusion than patients without LAE. On multivariable analysis, we found that among circulating inflammatory markers, only high VCAM-1 (OR: 9.13, 95% CI: 3.21-25.9) and sST2 (OR: 3.40, 95% CI: 1.68-6.86) AUC remained associated with LAE., Conclusions: High VCAM-1 and sST2 levels within the first 48 h are associated with LAE in AIS patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Fontaine, Leboube, Bochaton, Thibault, Amaz, Cho, Paccalet, Crola Da Silva, Duhamel, Buisson, Rascle, Bidaux, Ovize, Nighoghossian and Mechtouff.)- Published
- 2023
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35. SERCA2 phosphorylation at serine 663 is a key regulator of Ca 2+ homeostasis in heart diseases.
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Gonnot F, Boulogne L, Brun C, Dia M, Gouriou Y, Bidaux G, Chouabe C, Crola Da Silva C, Ducreux S, Pillot B, Kaczmarczyk A, Leon C, Chanon S, Perret C, Sciandra F, Dargar T, Gache V, Farhat F, Sebbag L, Bochaton T, Thibault H, Ovize M, Paillard M, and Gomez L
- Subjects
- Animals, Humans, Mice, Calcium metabolism, Homeostasis, Myocytes, Cardiac metabolism, Phosphorylation, Sarcoplasmic Reticulum metabolism, Sarcoplasmic Reticulum Calcium-Transporting ATPases metabolism, Myocardial Infarction metabolism, Myocardium metabolism
- Abstract
Despite advances in cardioprotection, new therapeutic strategies capable of preventing ischemia-reperfusion injury of patients are still needed. Here, we discover that sarcoplasmic/endoplasmic reticulum Ca
2+ ATPase (SERCA2) phosphorylation at serine 663 is a clinical and pathophysiological event of cardiac function. Indeed, the phosphorylation level of SERCA2 at serine 663 is increased in ischemic hearts of patients and mouse. Analyses on different human cell lines indicate that preventing serine 663 phosphorylation significantly increases SERCA2 activity and protects against cell death, by counteracting cytosolic and mitochondrial Ca2+ overload. By identifying the phosphorylation level of SERCA2 at serine 663 as an essential regulator of SERCA2 activity, Ca2+ homeostasis and infarct size, these data contribute to a more comprehensive understanding of the excitation/contraction coupling of cardiomyocytes and establish the pathophysiological role and the therapeutic potential of SERCA2 modulation in acute myocardial infarction, based on the hotspot phosphorylation level of SERCA2 at serine 663 residue., (© 2023. The Author(s).)- Published
- 2023
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36. Spatio-Temporal Characterization of Brain Inflammation in a Non-human Primate Stroke Model Mimicking Endovascular Thrombectomy.
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Becker G, Debatisse J, Rivière M, Crola Da Silva C, Beaudoin-Gobert M, Eker O, Wateau O, Cho TH, Wiart M, Tremblay L, Costes N, Mérida I, Redouté J, Léon C, Langlois JB, Le Bars D, Lancelot S, Nighoghossian N, Mechtouff L, and Canet-Soulas E
- Subjects
- Animals, Thrombectomy methods, Primates, Inflammation diagnostic imaging, Treatment Outcome, Ischemic Stroke diagnostic imaging, Ischemic Stroke surgery, Stroke therapy, Stroke drug therapy, Encephalitis, Brain Ischemia therapy, Brain Ischemia drug therapy
- Abstract
Reperfusion therapies in acute ischemic stroke have demonstrated their efficacy in promoting clinical recovery. However, ischemia/reperfusion injury and related inflammation remain a major challenge in patient clinical management. We evaluated the spatio-temporal evolution of inflammation using sequential clinical [
11 C]PK11195 PET-MRI in a non-human primate (NHP) stroke model mimicking endovascular thrombectomy (EVT) with a neuroprotective cyclosporine A (CsA) treatment. The NHP underwent a 110-min transient endovascular middle cerebral artery occlusion. We acquired [11 C]PK11195 dynamic PET-MR imaging at baseline, 7 and 30 days after intervention. Individual voxel-wise analysis was performed thanks to a baseline scan database. We quantified [11 C]PK11195 in anatomical regions and in lesioned areas defined on per-occlusion MR diffusion-weighted imaging and perfusion [15 O2 ]H2 OPET imaging. [11 C]PK11195 parametric maps showed a clear uptake overlapping the lesion core at D7, which further increased at D30. Voxel-wise analysis identified individuals with significant inflammation at D30, with voxels located within the most severe diffusion reduction area during occlusion, mainly in the putamen. The quantitative analysis revealed that thalamic inflammation lasted until D30 and was significantly reduced in the CsA-treated group compared to the placebo. In conclusion, we showed that chronic inflammation matched ADC decrease at occlusion time, a region exposed to an initial burst of damage-associated molecular patterns, in an NHP stroke model mimicking EVT. We described secondary thalamic inflammation and the protective effect of CsA in this region. We propose that major ADC drop in the putamen during occlusion may identify individuals who could benefit from early personalized treatment targeting inflammation., (© 2023. The Author(s).)- Published
- 2023
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37. Isolated Mitochondria State after Myocardial Ischemia-Reperfusion Injury and Cardioprotection: Analysis by Flow Cytometry.
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Crola Da Silva C, Baetz D, Védère M, Lo-Grasso M, Wehbi M, Chouabe C, Bidaux G, and Ferrera R
- Abstract
Rationale: Mitochondria are key organelles involved in cell survival and death during the acute phenomena of myocardial ischemia-reperfusion (i.e., myocardial infarction). To investigate the functions of isolated mitochondria such as calcium retention capacity, oxidative phosphorylation, and reactive oxygen species (ROS) production, already established methods are based on extramitochondrial measurements of the whole mitochondria population., Objective: The aim of this study was to develop a reliable and well-characterized method for multiparametric analysis of isolated single mitochondrion by flow cytometry (FC) in the context of myocardial infarction. The advantage of FC is the possibility to give a simultaneous analysis of morphological parameters (side and forward scatters: SSC and FSC) for each mitochondrion, combined with intramitochondrial measurements of several biological markers, such as ROS production or membrane potential (Δφm), using specific fluorescent probes., Methods and Results: For this study, a rat model of ischemia-reperfusion and a protective approach of post-conditioning using low reperfusion pressure was used. Thanks to the use of specific probes (NAO, MTR, TMRM, DilC1, and DHR123) combined with flow cytometry, we propose a method: (i) to identify mitochondrial populations of interest based on quality criteria (NAO/TMRM double staining); (ii) to monitor their morphological criteria, especially during swelling due to calcium overload; and (iii) to compare mitochondrial functions (membrane potential and ROS production) in different experimental groups. Applied to mitochondria from ischemic hearts, these measurements revealed that individual mitochondria are altered and that cardioprotection by low-pressure reperfusion reduces damage, as expected., Conclusions: Our results highlight FC as a reliable and sensitive method to investigate changes in mitochondrial functions and morphology in pathological conditions that disrupts their activity such as the case in ischemia-reperfusion. This methodological approach can be extended to other pathologies involving mitochondrial dysfunctions. Moreover, FC offers the possibility to work with very small amounts of isolated mitochondria, a factor that may limit the use of classical methods.
- Published
- 2023
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38. High-resolution synchrotron K-edge subtraction CT allows tracking and quantifying therapeutic cells and their scaffold in a rat model of focal cerebral injury and can serve as a reference for spectral photon counting CT.
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Tavakoli C, Cuccione E, Dumot C, Balegamire J, Si-Mohamed SA, Kim J, Crola-da-Silva C, Chevalier Y, Boussel L, Douek P, Cormode D, Elleaume H, Brun E, and Wiart M
- Subjects
- Rats, Animals, Contrast Media, Gold, Synchrotrons, Tomography, X-Ray Computed methods, Metal Nanoparticles, Iodine, Brain Injuries diagnostic imaging, Brain Injuries therapy
- Abstract
Background: The objective of this study was to demonstrate that synchrotron K-edge subtraction tomography (SKES-CT) can simultaneously track therapeutic cells and their encapsulating carrier, in vivo, in a rat model of focal brain injury using a dual-contrast agent approach. The second objective was to determine if SKES-CT could be used as a reference method for spectral photon counting tomography (SPCCT). Methods: Phantoms containing different concentrations of gold and iodine nanoparticles (AuNPS/INPs) were imaged with SKES-CT and SPCCT to assess their performances. A pre-clinical study was performed in rats with focal cerebral injury which intracerebrally received AuNPs-labelled therapeutic cells encapsulated in a INPs-labelled scaffold. Animals were imaged in vivo with SKES-CT and back-to-back with SPCCT. Results: SKES-CT revealed to be reliable for quantification of gold and iodine, whether alone or mixed. In the preclinical model, SKES-CT showed that AuNPs remained at the site of cell injection, while INPs expanded within and/or along the lesion border, suggesting dissociation of both components in the first days post-administration. Compared to SKES-CT, SPCCT was able to correctly locate gold, but not completely located iodine. When SKES-CT was used as reference, SPCCT gold quantification appeared very accurate both in vitro and in vivo . Iodine quantification by SPCCT was also quite accurate, albeit less so than for gold. Conclusion: We here provide the proof-of-concept that SKES-CT is a novel method of choice for performing dual-contrast agent imaging in the context of brain regenerative therapy. SKES-CT may also serve as ground truth for emerging technologies such as multicolour clinical SPCCT., Competing Interests: Competing Interests: Philips Healthcare was a partner in the Horizon 2020 grant no. 643694., (© The author(s).)
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- 2023
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39. Association of Blood Biomarkers of Inflammation With Penumbra Consumption After Mechanical Thrombectomy in Patients With Acute Ischemic Stroke.
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Mechtouff L, Debs N, Frindel C, Bani-Sadr A, Bochaton T, Paccalet A, Crola Da Silva C, Buisson M, Amaz C, Berthezene Y, Eker OF, Bouin M, de Bourguignon C, Mewton N, Ovize M, Bidaux G, Nighoghossian N, and Cho TH
- Subjects
- Humans, Thrombectomy methods, Treatment Outcome, Biomarkers, Inflammation diagnostic imaging, Brain Ischemia diagnostic imaging, Brain Ischemia surgery, Ischemic Stroke diagnostic imaging, Ischemic Stroke surgery, Stroke diagnostic imaging, Stroke surgery
- Abstract
Background and Objectives: The objective of this study was to assess the relationship between blood biomarkers of inflammation and lesion growth within the penumbra in acute ischemic stroke (AIS) patients treated with mechanical thrombectomy (MT)., Methods: The HIBISCUS-STROKE cohort enrolled patients admitted in the Lyon Stroke Center for an anterior circulation AIS treated with MT after brain MRI assessment. Lesion growth within the penumbra was assessed on day 6 MRI using a voxel-based nonlinear coregistration method and dichotomized into low and high according to the median value. C-reactive protein, interleukin (IL)-6, IL-8, IL-10, monocyte chemoattractant protein-1, soluble tumor necrosis factor receptor I, soluble form suppression of tumorigenicity 2 (sST2), soluble P-selectin, vascular cellular adhesion molecule-1, and matrix metalloproteinase-9 were measured in sera at 4 time points within the first 48 hours. Reperfusion was considered as successful if Thrombolysis in Cerebral Infarction score was 2b/2c/3. A multiple logistic regression model was performed to detect any association between area under the curve (AUC) of these biomarkers within the first 48 hours and a high lesion growth within the penumbra., Results: Ninety patients were included. The median lesion growth within the penumbra was 2.3 (0.7-6.2) mL. On multivariable analysis, a high sST2 AUC (OR 3.77, 95% CI 1.36-10.46), a high baseline DWI volume (OR 3.65, 95% CI 1.32-10.12), and a lack of successful reperfusion (OR 0.19, 95% CI 0.04-0.92) were associated with a high lesion growth within the penumbra. When restricting analyses to patients with successful reperfusion (n = 76), a high sST2 AUC (OR 5.03, 95% CI 1.64-15.40), a high baseline DWI volume (OR 3.74, 95% CI 1.22-11.53), and a high penumbra volume (OR 3.25, 95% CI 1.10-9.57) remained associated with a high lesion growth within the penumbra., Discussion: High sST2 levels within the first 48 hours are associated with a high lesion growth within the penumbra., (© 2022 American Academy of Neurology.)
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- 2022
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40. Impact of Age on Systemic Inflammatory Profile of Patients With ST-Segment-Elevation Myocardial Infarction and Acute Ischemic Stroke.
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Bochaton T, Leboube S, Paccalet A, Crola Da Silva C, Buisson M, Mewton N, Amaz C, Varillon Y, Bonnefoy-Cudraz E, Rioufol G, Cho TH, Ovize M, Bidaux G, Nighoghossian N, and Mechtouff L
- Subjects
- Aged, Biomarkers analysis, C-Reactive Protein, Humans, Interleukin-6, Middle Aged, Percutaneous Coronary Intervention, Stroke therapy, Ischemic Stroke immunology, Ischemic Stroke therapy, ST Elevation Myocardial Infarction immunology, ST Elevation Myocardial Infarction therapy, Systemic Inflammatory Response Syndrome immunology
- Abstract
Background: Aging is associated with a chronic low-grade inflammatory state. This condition may affect the acute inflammatory response involved in ST-segment-elevation myocardial infarction (STEMI) or acute ischemic stroke (AIS). We sought to compare the profile of a set of circulating inflammatory markers between young and older patients admitted for STEMI or AIS., Methods: HIBISCUS-STEMI (Cohort of Patients to Identify Biological and Imaging Markers of Cardiovascular Outcomes in ST Elevation Myocardial Infarction) and HIBISCUS-STROKE (Cohort of Patients to Identify Biological and Imaging Markers of Cardiovascular Outcomes in Stroke) are 2 cohort studies that enrolled patients with STEMI treated with primary percutaneous coronary intervention in the cardiac intensive care unit of Lyon and patients with AIS treated with mechanical thrombectomy in the Lyon Stroke Center, respectively from 2016 to 2019. Patients were classified as older if they were ≥65 years and as young if they were <65 years. In both cohorts, CRP (C-reactive protein), IL (interleukin)-6, IL-8, IL-10, MCP (monocyte chemoattractant protein), sTNF-RI (soluble tumor necrosis factor receptor I), sST2 (soluble form suppression of tumorigenicity 2), and VCAM-1 (vascular cellular adhesion molecule-1) were measured on serum collected at 5 time points using enzyme-linked immunosorbent assay. A multiple logistic regression model was performed to detect an association between area under the curve of circulating inflammatory markers within the first 48 hours and older age., Results: A total of 260 patients with STEMI and 164 patients with AIS were included. Of them, there were 76 (29%) and 105 (64%) older patients with STEMI and AIS, respectively. Following multivariable analysis, a high area under the curve of IL-6 and sTNF-RI, a low lymphocyte count, and a high neutrophil-lymphocyte ratio at 24 hours were associated with older age in patients with STEMI and AIS., Conclusions: Older patients had higher IL-6 and sTFN-RI levels within the first 48 hours associated with a lower lymphocyte count and a higher neutrophil-lymphocyte ratio at 24 hours in both cohorts.
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- 2022
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41. Simultaneous assessment of microcalcifications and morphological criteria of vulnerability in carotid artery plaque using hybrid 18 F-NaF PET/MRI.
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Mechtouff L, Sigovan M, Douek P, Costes N, Le Bars D, Mansuy A, Haesebaert J, Bani-Sadr A, Tordo J, Feugier P, Millon A, Luong S, Si-Mohamed S, Collet-Benzaquen D, Canet-Soulas E, Bochaton T, Crola Da Silva C, Paccalet A, Magne D, Berthezene Y, and Nighoghossian N
- Subjects
- Humans, Magnetic Resonance Imaging, Positron-Emission Tomography methods, Sodium Fluoride, Calcinosis diagnostic imaging, Carotid Stenosis diagnostic imaging, Plaque, Atherosclerotic diagnostic imaging
- Abstract
Background: Previous studies have suggested the role of microcalcifications in plaque vulnerability. This exploratory study sought to assess the potential of hybrid positron-emission tomography (PET)/magnetic resonance imaging (MRI) using
18 F-sodium fluoride (18 F-NaF) to check simultaneously18 F-NaF uptake, a marker of microcalcifications, and morphological criteria of vulnerability., Methods and Results: We included 12 patients with either recently symptomatic or asymptomatic carotid stenosis. All patients underwent18 F-NaF PET/MRI.18 F-NaF target-to-background ratio (TBR) was measured in culprit and nonculprit (including contralateral plaques of symptomatic patients) plaques as well as in other arterial walls. Morphological criteria of vulnerability were assessed on MRI. Mineral metabolism markers were also collected.18 F-NaF uptake was higher in culprit compared to nonculprit plaques (median TBR 2.6 [2.2-2.8] vs 1.7 [1.3-2.2]; P = 0.03) but was not associated with morphological criteria of vulnerability on MRI. We found a positive correlation between18 F-NaF uptake and calcium plaque volume and ratio but not with circulating tissue-nonspecific alkaline phosphatase (TNAP) activity and inorganic pyrophosphate (PPi) levels.18 F-NaF uptake in the other arterial walls did not differ between symptomatic and asymptomatic patients., Conclusions:18 F-NaF PET/MRI may be a promising tool for providing additional insights into the plaque vulnerability., (© 2020. American Society of Nuclear Cardiology.)- Published
- 2022
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42. Prognosis value of serum soluble ST2 level in acute ischemic stroke and STEMI patients in the era of mechanical reperfusion therapy.
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Mechtouff L, Paccalet A, Crola Da Silva C, Buisson M, Mewton N, Amaz C, Bonnefoy-Cudraz E, Leboube S, Cho TH, Nighoghossian N, Ovize M, and Bochaton T
- Subjects
- Humans, Prognosis, Reperfusion, Interleukin-1 Receptor-Like 1 Protein blood, Ischemic Stroke, ST Elevation Myocardial Infarction surgery
- Abstract
Background: Soluble form suppression of tumorigenicity 2 (sST2) is known to have prognostic value in ST-elevation myocardial infarction (STEMI) and could impact mortality after acute ischemic stroke (AIS). However, before considering sST2 as a therapeutic target, the kinetics of release and its association with adverse clinical events in both STEMI and AIS patients have to be determined., Methods: We prospectively enrolled 251 STEMI patients, treated with primary percutaneous coronary intervention, and 152 AIS patients treated with mechanical thrombectomy. We evaluated the level of sST2 in patient sera at five time point (admission, 4, 24, 48 h and 1 month from admission for STEMI patients and admission, 6, 24, 48 h and 3 months from admission for AIS patients). Major adverse clinical events (MACE) (all-cause death, acute myocardial infarction, stroke or hospitalization for heart failure) in STEMI patients and all-cause death in AIS patients were recorded during a 12-month follow-up., Results: Mean age of the study population was 59 ± 12 and 69 ± 15 years in STEMI and AIS patients, respectively. In STEMI patients, sST2 peaked 24 h after admission (25.5 ng/mL interquartile range (IQR) [14.9-29.1]) whereas an earlier and lower peak was observed in AIS patients (16.8 ng/mL IQR [15.2-18.3] at 6 h). Twenty-five (10.0%) STEMI patients experienced a MACE and 12 (7.9%) AIS patients had all-cause death within the first 12 months. A high level of sST2 at 24 h was associated with MACE in STEMI patients (hazard ratio (HR) = 2.5; 95% confidence interval (CI) [1.1-5.6], p = 0.03) and all-cause death in AIS patients (HR = 11.7; 95% CI [3.8-36.2], p < 0.01) within the first 12 months., Conclusions: The study highlights that sST2 levels at 24 h are associated with an increased risk to adverse clinical events in both diseases., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)
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- 2022
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43. Measurement of fish freshness: Flow cytometry analysis of isolated muscle mitochondria.
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Soret M, Bouchendhomme T, Cleach J, Jouy N, Crola Da Silva C, Devin A, Grard T, and Lencel P
- Subjects
- Animals, Flow Cytometry, Mitochondria, Mitochondria, Muscle, Seafood analysis, Bass
- Abstract
Mitochondria are real sensors of the physiological status of tissues. After the death of an animal, they maintain physiological activity for several days. This activity is highly dependent on the availability of nutrients in the tissue. In this study, flow cytometry was used to measure the membrane potential of mitochondria isolated from European seabass (Dicentrarchus labrax) red muscle stored in ice for seven days in order to characterize fish freshness. Two probes, TMRM and Rhodamine 123, were used to measure mitochondrial potential. During the first few days (D0 to D3), isolated mitochondria maintained high potential, and then lost their potential (from D3 to D5), but were always re-polarizable after addition of substrates (glutamate, malate and succinate). From D7, the mitochondria were more strongly depolarized and were difficult to repolarize by the substrates. Using flow cytometry, we demonstrated that mitochondria were an excellent marker to confirm seabass freshness., (Copyright © 2021 Elsevier Ltd. All rights reserved.)
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- 2022
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44. Cooling Uncouples Differentially ROS Production from Respiration and Ca 2+ Homeostasis Dynamic in Brain and Heart Mitochondria.
- Author
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Stevic N, Maalouf J, Argaud L, Gallo-Bona N, Lo Grasso M, Gouriou Y, Gomez L, Crola Da Silva C, Ferrera R, Ovize M, Cour M, and Bidaux G
- Subjects
- Animals, Homeostasis, Mice, Reactive Oxygen Species, Respiration, Brain, Mitochondria, Heart
- Abstract
Hypothermia provides an effective neuro and cardio-protection in clinical settings implying ischemia/reperfusion injury (I/R). At the onset of reperfusion, succinate-induced reactive oxygen species (ROS) production, impaired oxidative phosphorylation (OXPHOS), and decreased Ca
2+ retention capacity (CRC) concur to mitochondrial damages. We explored the effects of temperature from 6 to 37 °C on OXPHOS, ROS production, and CRC, using isolated mitochondria from mouse brain and heart. Oxygen consumption and ROS production was gradually inhibited when cooling from 37 to 6 °C in brain mitochondria (BM) and heart mitochondria (HM). The decrease in ROS production was gradual in BM but steeper between 31 and 20 °C in HM. In respiring mitochondria, the gradual activation of complex II, in addition of complex I, dramatically enhanced ROS production at all temperatures without modifying respiration, likely because of ubiquinone over-reduction. Finally, CRC values were linearly increased by cooling in both BM and HM. In BM, the Ca2+ uptake rate by the mitochondrial calcium uniporter (MCU) decreased by 2.7-fold between 25 and 37 °C, but decreased by 5.7-fold between 25 and 37 °C in HM. In conclusion, mild cold (25-37 °C) exerts differential inhibitory effects by preventing ROS production, by reverse electron transfer (RET) in BM, and by reducing MCU-mediated Ca2+ uptake rate in BM and HM.- Published
- 2022
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45. A lower admission level of interleukin-6 is associated with first-pass effect in ischemic stroke patients.
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Mechtouff L, Bochaton T, Paccalet A, Crola Da Silva C, Buisson M, Amaz C, Derex L, Ong E, Berthezene Y, Dufay N, Ovize M, Mewton N, Cho TH, Nighoghossian N, and Eker OF
- Subjects
- Aged, Humans, Interleukin-6, Retrospective Studies, Thrombectomy methods, Treatment Outcome, Brain Ischemia diagnostic imaging, Ischemic Stroke, Stroke diagnostic imaging, Stroke therapy
- Abstract
Background: First-pass effect (FPE) defined as a complete or near-complete reperfusion achieved after a single thrombectomy pass is predictive of favorable outcome in acute ischemic stroke (AIS) patients. We aimed to assess whether admission levels of inflammatory markers are associated with FPE., Methods: HIBISCUS-STROKE (CoHort of Patients to Identify Biological and Imaging markerS of CardiovascUlar Outcomes in Stroke) includes AIS patients with large vessel occlusion treated with mechanical thrombectomy following brain MRI. C-reactive protein, interleukin (IL)-6, IL-8, IL-10, monocyte chemoattractant protein-1, soluble tumor necrosis factor receptor I, soluble form suppression of tumorigenicity 2, matrix metalloproteinase-9 (MMP-9), soluble P-selectin, and vascular cellular adhesion molecule-1 were measured in admission sera using an ELISA assay. FPE was defined as a complete or near-complete reperfusion (thrombolysis in cerebral infarction scale (TICI) 2c or 3) after the first pass. A multivariate logistic regression analysis was performed to assess independent factors associated with FPE., Results: A total of 151 patients were included. Among them, 43 (28.5%) patients had FPE. FPE was associated with low admission levels of IL-6, MMP-9, and platelet count, an older age, lack of hypertension, lack of tandem occlusion, a shorter thrombus length, and a reduced procedural time. Following multivariate analysis, a low admission level of IL-6 was associated with FPE (OR 0.66, 95% CI 0.46 to 0.94). Optimal cut-off of IL-6 level for distinguishing FPE from non-FPE was 3.0 pg/mL (sensitivity 92.3%, specificity 42.3%)., Conclusion: A lower admission level of IL-6 is associated with FPE., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.)
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- 2022
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46. Brain virtual histology with X-ray phase-contrast tomography Part I: whole-brain myelin mapping in white-matter injury models.
- Author
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Chourrout M, Rositi H, Ong E, Hubert V, Paccalet A, Foucault L, Autret A, Fayard B, Olivier C, Bolbos R, Peyrin F, Crola-da-Silva C, Meyronet D, Raineteau O, Elleaume H, Brun E, Chauveau F, and Wiart M
- Abstract
White-matter injury leads to severe functional loss in many neurological diseases. Myelin staining on histological samples is the most common technique to investigate white-matter fibers. However, tissue processing and sectioning may affect the reliability of 3D volumetric assessments. The purpose of this study was to propose an approach that enables myelin fibers to be mapped in the whole rodent brain with microscopic resolution and without the need for strenuous staining. With this aim, we coupled in-line (propagation-based) X-ray phase-contrast tomography (XPCT) to ethanol-induced brain sample dehydration. We here provide the proof-of-concept that this approach enhances myelinated axons in rodent and human brain tissue. In addition, we demonstrated that white-matter injuries could be detected and quantified with this approach, using three animal models: ischemic stroke, premature birth and multiple sclerosis. Furthermore, in analogy to diffusion tensor imaging (DTI), we retrieved fiber directions and DTI-like diffusion metrics from our XPCT data to quantitatively characterize white-matter microstructure. Finally, we showed that this non-destructive approach was compatible with subsequent complementary brain sample analysis by conventional histology. In-line XPCT might thus become a novel gold-standard for investigating white-matter injury in the intact brain. This is Part I of a series of two articles reporting the value of in-line XPCT for virtual histology of the brain; Part II shows how in-line XPCT enables the whole-brain 3D morphometric analysis of amyloid- β (A β ) plaques., Competing Interests: The authors declare no conflicts of interest., (© 2022 Optical Society of America under the terms of the OSA Open Access Publishing Agreement.)
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- 2022
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47. Serum Soluble Tumor Necrosis Factor Receptors 1 and 2 Are Early Prognosis Markers After ST-Segment Elevation Myocardial Infarction.
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Paccalet A, Crola Da Silva C, Mechtouff L, Amaz C, Varillon Y, de Bourguignon C, Cartier R, Prieur C, Tomasevic D, Genot N, Leboube S, Derimay F, Rioufol G, Bonnefoy-Cudraz E, Mewton N, Ovize M, Bidaux G, and Bochaton T
- Abstract
Background: As inflammation following ST-segment elevation myocardial infarction (STEMI) is both beneficial and deleterious, there is a need to find new biomarkers of STEMI severity. Objective: We hypothesized that the circulating concentration of the soluble tumor necrosis factor α receptors 1 and 2 (sTNFR1 and sTNFR2) might predict clinical outcomes in STEMI patients. Methods: We enrolled into a prospective cohort 251 consecutive STEMI patients referred to our hospital for percutaneous coronary intervention revascularization. Blood samples were collected at five time points: admission and 4, 24, 48 h, and 1 month after admission to assess sTNFR1 and sTNFR2 serum concentrations. Patients underwent cardiac magnetic resonance imaging at 1 month. Results: sTNFR1 concentration increased at 24 h with a median of 580.5 pg/ml [95% confidence interval (CI): 534.4-645.6]. sTNFR2 increased at 48 h with a median of 2,244.0 pg/ml [95% CI: 2090.0-2,399.0]. Both sTNFR1 and sTNFR2 peak levels were correlated with infarct size and left ventricular end-diastolic volume and inversely correlated with left ventricular ejection fraction. Patients with sTNFR1 or sTNFR2 concentration above the median value were more likely to experience an adverse clinical event within 24 months after STEMI [hazards ratio (HR): 8.8, 95% CI: 4.2-18.6, p < 0.0001 for sTNFR1; HR: 6.1, 95% CI: 2.5 -10.5, p = 0.0003 for sTNFR2]. Soluble TNFR1 was an independent predictor of major adverse cardiovascular events and was more powerful than troponin I ( p = 0.04 as compared to the troponin AUC). Conclusion: The circulating sTNFR1 and sTNFR2 are inflammatory markers of morphological and functional injury after STEMI. sTNFR1 appears as an early independent predictor of clinical outcomes in STEMI patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Paccalet, Crola Da Silva, Mechtouff, Amaz, Varillon, de Bourguignon, Cartier, Prieur, Tomasevic, Genot, Leboube, Derimay, Rioufol, Bonnefoy-Cudraz, Mewton, Ovize, Bidaux and Bochaton.)
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- 2021
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48. Cardiomyocyte Protection by Hibernating Brown Bear Serum: Toward the Identification of New Protective Molecules Against Myocardial Infarction.
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Givre L, Crola Da Silva C, Swenson JE, Arnemo JM, Gauquelin-Koch G, Bertile F, Lefai E, and Gomez L
- Abstract
Ischemic heart disease remains one of the leading causes of death worldwide. Despite intensive research on the treatment of acute myocardial infarction, no effective therapy has shown clinical success. Therefore, novel therapeutic strategies are required to protect the heart from reperfusion injury. Interestingly, despite physical inactivity during hibernation, brown bears ( Ursus arctos ) cope with cardiovascular physiological conditions that would be detrimental to humans. We hypothesized that bear serum might contain circulating factors that could provide protection against cell injury. In this study, we sought to determine whether addition of bear serum might improve cardiomyocyte survival following hypoxia-reoxygenation. Isolated mouse cardiomyocytes underwent 45 min of hypoxia followed by reoxygenation. At the onset of reoxygenation, cells received fetal bovine serum (FBS; positive control), summer (SBS) or winter bear serum (WBS), or adult serums of other species, as indicated. After 2 h of reoxygenation, propidium iodide staining was used to evaluate cell viability by flow cytometry. Whereas, 0.5% SBS tended to decrease reperfusion injury, 0.5% WBS significantly reduced cell death, averaging 74.04 ± 7.06% vs. 79.20 ± 6.53% in the FBS group. This cardioprotective effect was lost at 0.1%, became toxic above 5%, and was specific to the bear. Our results showed that bear serum exerts a therapeutic effect with an efficacy threshold, an optimal dose, and a toxic effect on cardiomyocyte viability after hypoxia-reoxygenation. Therefore, the bear serum may be a potential source for identifying new therapeutic molecules to fight against myocardial reperfusion injury and cell death in general., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Givre, Crola Da Silva, Swenson, Arnemo, Gauquelin-Koch, Bertile, Lefai and Gomez.)
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- 2021
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49. Cortical inflammation and brain signs of high-risk atherosclerosis in a non-human primate model.
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Di Cataldo V, Debatisse J, Piraquive J, Géloën A, Grandin C, Verset M, Taborik F, Labaronne E, Loizon E, Millon A, Mury P, Pialoux V, Serusclat A, Lamberton F, Ibarrola D, Lavenne F, Le Bars D, Troalen T, Confais J, Crola Da Silva C, Mechtouff L, Contamin H, Fayad ZA, and Canet-Soulas E
- Abstract
Atherosclerosis is a chronic systemic inflammatory disease, inducing cardiovascular and cerebrovascular acute events. A role of neuroinflammation is suspected, but not yet investigated in the gyrencephalic brain and the related activity at blood-brain interfaces is unknown. A non-human primate model of advanced atherosclerosis was first established using longitudinal blood samples, multimodal imaging and gene analysis in aged animals. Non-human primate carotid lesions were compared with human carotid endarterectomy samples. During the whole-body imaging session, imaging of neuroinflammation and choroid plexus function was performed. Advanced plaques were present in multiple sites, premature deaths occurred and downstream lesions (myocardial fibrosis, lacunar stroke) were present in this model. Vascular lesions were similar to in humans: high plaque activity on PET and MRI imaging and systemic inflammation (high plasma C-reactive protein levels: 42 ± 14 µg/ml). We also found the same gene association (metabolic, inflammatory and anti-inflammatory markers) as in patients with similar histological features. Metabolic imaging localized abnormal brain glucose metabolism in the frontal cortex. It corresponded to cortical neuro-inflammation (PET imaging) that correlated with C-reactive protein level. Multimodal imaging also revealed pronounced choroid plexus function impairment in aging atherosclerotic non-human primates. In conclusion, multimodal whole-body inflammation exploration at the vascular level and blood-brain interfaces identified high-risk aging atherosclerosis. These results open the way for systemic and central inflammation targeting in atherosclerosis in the new era of immunotherapy., (© The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.)
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- 2021
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50. Myocardial Ischemia-Reperfusion and Diabetes: Lessons Learned From Bedside to Bench.
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Dia M, Paccalet A, Pillot B, Leon C, Ovize M, Crola Da Silva C, Bochaton T, and Paillard M
- Abstract
In front of the failure to translate from bench to bedside cardioprotective drugs against myocardial ischemia-reperfusion, research scientists are currently revising their animal models. Owing to its growing incidence nowadays, type 2 diabetes (T2D) represents one of the main risk factors of co-morbidities in myocardial infarction. However, discrepancies exist between reported animal and human studies. Our aim was here to compare the impact of diabetes on cell death after cardiac ischemia-reperfusion in a human cohort of ST-elevation myocardial infarction (STEMI) patients with a diet-induced mouse model of T2D, using a high-fat high-sucrose diet for 16 weeks (HFHSD). Interestingly, a small fraction (<14%) of patients undergoing a myocardial infarct were diabetic, but treated, and did not show a bigger infarct size when compared to non-diabetic patients. On the contrary, HFHSD mice displayed an increased infarct size after an in vivo cardiac ischemia-reperfusion, together with an increased cell death after an in vitro hypoxia-reoxygenation on isolated cardiomyocytes. To mimic the diabetic patients' medication profile, 6 weeks of oral gavage with Metformin was performed in the HFHSD mouse group. Metformin treatment of the HFHSD mice led to a similar extent of lower cell death after hypoxia-reoxygenation as in the standard diet group, compared to the HFHSD cardiomyocytes. Altogether, our data highlight that due to their potential protective effect, anti-diabetic medications should be included in pre-clinical study of cardioprotective approaches. Moreover, since diabetic patients represent only a minor fraction of the STEMI patients, diabetic animal models may not be the most suitable translatable model to humans, unlike aging that appears as a common feature of all infarcted patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Dia, Paccalet, Pillot, Leon, Ovize, Crola Da Silva, Bochaton and Paillard.)
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- 2021
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