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3 results on '"Clement, Delacroix"'

1. FIBER-ML, an Open-Source Supervised Machine Learning Tool for Quantification of Fibrosis in Tissue Sections

Author

Caterina Facchin, Anais Certain, Thulaciga Yoganathan, Clement Delacroix, Alicia Arevalo Garcia, François Gaillard, Olivia Lenoir, Pierre-Louis Tharaux, Bertrand Tavitian, Daniel Balvay, Paris-Centre de Recherche Cardiovasculaire (PARCC (UMR_S 970/ U970)), Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), and Lenoir, Olivia

Subjects
Male, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Fibrosis, Rats, Pathology and Forensic Medicine, Mice, Takotsubo Cardiomyopathy, [SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Image Processing, Computer-Assisted, Animals, Humans, Female, Supervised Machine Learning, Renal Insufficiency, Chronic, Software
Abstract

International audience; Pathologic fibrosis is a major hallmark of tissue insult in many chronic diseases. Although the amount of fibrosis is recognized as a direct indicator of the extent of disease, there is no consentaneous method for its quantification in tissue sections. This study tested FIBER-ML, a semi-automated, open-source freeware that uses a machine-learning approach to quantify fibrosis automatically after a short user-controlled learning phase. Fibrosis was quantified in sirius red-stained tissue sections from two fibrogenic animal models: acute stress-induced cardiomyopathy in rats (Takotsubo syndrome-like) and HIV-induced nephropathy in mice (chronic kidney disease). The quantitative results of FIBER-ML software version 1.0 were compared with those of ImageJ in Takotsubo syndrome, and with those of inForm in chronic kidney disease. Intra- and inter-operator and inter-software correlation and agreement were assessed. All correlations were excellent (>0.95) in both data sets. The values of discriminatory power between the pathologic and healthy groups were 0.8), while inter-operator and inter-software agreement ranged from moderate to good (>0.7). FIBER-ML performed in a fast and user-friendly manner, with reproducible and consistent quantification of fibrosis in tissue sections. It offers an open-source alternative to currently used software, including quality control and file management.

Published
2022

2. Cytotoxic CD8+ T Cells Promote Granzyme B-Dependent Adverse Post-Ischemic Cardiac Remodeling

Author

Icia Santos Zas, Jeremie Lemarie, Ivana Zlatanova, Marine Cachanado, Jean-Christophe Seghezzi, Hakim Benamer, Pascal Goube, Marie Vandestienne, Raphael Cohen, Maya Ezzo, Vincent Duval, Yujiao Zhang, Gin-Bo Su, Alain Bizé, Lucien Sambin, Philippe Bonnin, Maxime Branchereau, Christophe Heymes, Corinne Tanchot, Jose Vilar, Clement Delacroix, Jean-Sebastien Hulot, Clement Cochain, patrick bruneval, Nicolas Danchin, Alain Tedgui, Ziad Mallat, Tabassome Simon, Bijan Ghaleh, Jean-sébastien Silvestre, Hafid Ait-Oufella, Paris-Centre de Recherche Cardiovasculaire (PARCC (UMR_S 970/ U970)), Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Pôle de Pharmacie - Santé Publique - Information médicale [Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre Hospitalier Compiègne-Noyon (CHCN), Centre Hospitalier Compiègne-Noyon, Institut Cardiovasculaire Paris Sud, Centre Jacques Cartier, Centre Hospitalier Sud Francilien [Corbeil-Essonnes] (CH Sud Francilien), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Institut des Vaisseaux et du Sang, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Lariboisière-Fernand-Widal [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), University of Würzburg = Universität Würzburg, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), University of Cambridge [UK] (CAM), Service de Réanimation Médicale [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Pôle de Pharmacie - Santé Publique - Information médicale [CHU Saint-Antoine], CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Santos-Zas, Icia [0000-0002-0310-9074], Su, Jin-Bo [0000-0002-1823-8928], Bonnin, Philippe [0000-0003-3184-3740], Vilar, José [0000-0002-9136-7726], Tedgui, Alain [0000-0002-7229-4875], Ghaleh, Bijan [0000-0003-0061-5462], Silvestre, Jean-Sébastien [0000-0003-3962-2205], Ait-Oufella, Hafid [0000-0002-2955-0183], Apollo - University of Cambridge Repository, and HAL-SU, Gestionnaire

Subjects
Male, 692/4019/592/75/230, Swine, Science, Myocardial Infarction, Apoptosis, 13/106, Heart failure, CD8-Positive T-Lymphocytes, 13, Granzymes, 13/2, Mice, 13/1, 13/21, Animals, Humans, Lymphocytes, cardiovascular diseases, 631/250/1619, Homeodomain Proteins, Mice, Knockout, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Ventricular Remodeling, Myocardium, article, Heart, 3. Good health, Mice, Inbred C57BL, 13/31, Disease Models, Animal, 13/51, cardiovascular system, Female, Transcriptome, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Acute myocardial infarction (MI) is a common condition responsible for heart failure and sudden death. Here, we show that following acute MI in mice, CD8+ T lymphocytes are recruited and activated in the ischemic heart tissue, and release Granzyme B leading to cardiomyocyte apoptosis, adverse ventricular remodeling and deterioration of myocardial function. Depletion of CD8+ T lymphocytes decreases apoptosis within the ischemic myocardium, hampers inflammatory response, limits myocardial injury and improves heart function. These effects are recapitulated in mice with Granzyme B-deficient CD8+ T cells. The protective effect of CD8 depletion on heart function was confirmed by using a model of ischemia/reperfusion in pigs. Finally, we reveal that elevated circulating levels of Granzyme B in patients with acute MI predict increased risk of death at 1-year follow-up. Our work unravels an unsuspected deleterious role of CD8+ T lymphocytes following acute ischemia, and identifies novel therapeutic strategy targeting pathogenic CD8+ T lymphocytes in the setting of acute MI.

Published
2020

3. Cytotoxic CD8

Author

Icia, Santos-Zas, Jeremie, Lemarié, Ivana, Zlatanova, Marine, Cachanado, Jean-Christophe, Seghezzi, Hakim, Benamer, Pascal, Goube, Marie, Vandestienne, Raphael, Cohen, Maya, Ezzo, Vincent, Duval, Yujiao, Zhang, Jin-Bo, Su, Alain, Bizé, Lucien, Sambin, Philippe, Bonnin, Maxime, Branchereau, Christophe, Heymes, Corinne, Tanchot, José, Vilar, Clement, Delacroix, Jean-Sebastien, Hulot, Clement, Cochain, Patrick, Bruneval, Nicolas, Danchin, Alain, Tedgui, Ziad, Mallat, Tabassome, Simon, Bijan, Ghaleh, Jean-Sébastien, Silvestre, and Hafid, Ait-Oufella

Subjects
Heart Failure, Homeodomain Proteins, Male, Mice, Knockout, Ventricular Remodeling, Swine, Myocardium, Myocardial Infarction, Apoptosis, Heart, CD8-Positive T-Lymphocytes, Granzymes, Article, Mice, Inbred C57BL, Disease Models, Animal, Mice, Animals, Humans, Female, cardiovascular diseases, Lymphocytes, Transcriptome
Abstract

Acute myocardial infarction is a common condition responsible for heart failure and sudden death. Here, we show that following acute myocardial infarction in mice, CD8+ T lymphocytes are recruited and activated in the ischemic heart tissue and release Granzyme B, leading to cardiomyocyte apoptosis, adverse ventricular remodeling and deterioration of myocardial function. Depletion of CD8+ T lymphocytes decreases apoptosis within the ischemic myocardium, hampers inflammatory response, limits myocardial injury and improves heart function. These effects are recapitulated in mice with Granzyme B-deficient CD8+ T cells. The protective effect of CD8 depletion on heart function is confirmed by using a model of ischemia/reperfusion in pigs. Finally, we reveal that elevated circulating levels of GRANZYME B in patients with acute myocardial infarction predict increased risk of death at 1-year follow-up. Our work unravels a deleterious role of CD8+ T lymphocytes following acute ischemia, and suggests potential therapeutic strategies targeting pathogenic CD8+ T lymphocytes in the setting of acute myocardial infarction., Immune cells contribute to adverse remodeling following myocardial infarction. Here the authors show in mice and pigs that CD8+ lymphocytes release Granzyme B in the infarcted heart leading to cardiomyocyte death, enhanced inflammation and deterioration of cardiac function.

Published
2020

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