Search

Your search keyword '"Chantal Kazazian"' showing total 4 results
Start Over Author "Chantal Kazazian"
4 results on '"Chantal Kazazian"'

1. Reduced NOV/CCN3 Expression Limits Inflammation and Interstitial Renal Fibrosis after Obstructive Nephropathy in Mice.

Author

Pierre-Olivier Marchal, Panagiotis Kavvadas, Ahmed Abed, Chantal Kazazian, Florence Authier, Haruhiko Koseki, Shuichi Hiraoka, Jean-Jacques Boffa, Cécile Martinerie, and Christos E Chadjichristos

Subjects
Medicine, Science
Abstract

The main hallmark of chronic kidney disease (CKD) is excessive inflammation leading to interstitial tissue fibrosis. It has been recently reported that NOV/CCN3 could be involved in kidney damage but its role in the progression of nephropathies is poorly known. NOV/CCN3 is a secreted multifunctional protein belonging to the CCN family involved in different physiological and pathological processes such as angiogenesis, inflammation and cancers. The purpose of our study was to determine the role of NOV/CCN3 in renal inflammation and fibrosis related to primitive tubulointerstitial injury. After unilateral ureteral obstruction (UUO), renal histology and real-time PCR were performed in NOV/CCN3-/- and wild type mice. NOV/CCN3 mRNA expression was increased in the obstructed kidneys in the early stages of the obstructive nephropathy. Interestingly, plasmatic levels of NOV/CCN3 were strongly induced after 7 days of UUO and the injection of recombinant NOV/CCN3 protein in healthy mice significantly increased CCL2 mRNA levels. Furthermore, after 7 days of UUO NOV/CCN3-/- mice displayed reduced proinflammatory cytokines and adhesion markers expression leading to restricted accumulation of interstitial monocytes, in comparison with their wild type littermates. Consequently, in NOV/CCN3-/- mice interstitial renal fibrosis was blunted after 15 days of UUO. In agreement with our experimental data, NOV/CCN3 expression was highly increased in biopsies of patients with tubulointerstitial nephritis. Thus, the inhibition of NOV/CCN3 may represent a novel target for the progression of renal diseases.

Published
2015
Full Text
View/download PDF

2. NOV/CCN3: A new adipocytokine involved in obesity-associated insulin resistance

Author

Haruhiko Koseki, Martine Auclair, Marthe Moldes, Christos E. Chadjichristos, Guillaume Dorothée, Bénédicte Antoine, R.G. Denis, Tatiana Ledent, Pierre-Olivier Marchal, Chantal Kazazian, Serge Luquet, Bruno Fève, B. Blondeau, Marie Garcia, Cécile Martinerie, Shuichi Hiraoka, Thi Thu Huong Do, Adrien Beisseiche, Maria Fesatidou, M. Buyse, Centre de Recherche Saint-Antoine (UMRS893), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Institute of cardiometabolism and nutrition (ICAN), Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de Pharmacie [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), Barrières physiologiques et réponses thérapeutiques, Université Paris-Sud - Paris 11 (UP11), Centre de Recherche des Cordeliers (CRC), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Environmental Molecular Biology Laboratory (RIKEN), RIKEN - Institute of Physical and Chemical Research [Japon] (RIKEN), Kobe Pharmaceutical University, CHU Tenon [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Unité de Biologie Fonctionnelle et Adaptative (BFA (UMR_8251 / U1133)), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service d'Endocrinologie, diabétologie et endocrinologie de la reproduction [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), Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Research Unit on Cardiovascular and Metabolic Diseases (ICAN), Centre de Recherche Saint-Antoine (CRSA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Système immunitaire et neuroinflammation [CRSA], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche Saint-Antoine ( CR Saint-Antoine ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ), Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Institute of cardiometabolism and nutrition ( ICAN ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Assistance publique - Hôpitaux de Paris (AP-HP)-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -CHU Pitié-Salpêtrière [APHP], Assistance publique - Hôpitaux de Paris (AP-HP)-CHU Saint-Antoine [APHP], Université Paris-Sud - Paris 11 ( UP11 ), Centre de Recherche des Cordeliers ( CRC ), Université Paris Diderot - Paris 7 ( UPD7 ) -École pratique des hautes études ( EPHE ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Environmental Molecular Biology Laboratory ( RIKEN ), RIKEN, CHU Tenon [APHP], Biologie Fonctionnelle et Adaptative ( BFA ), Université Paris Diderot - Paris 7 ( UPD7 ) -Centre National de la Recherche Scientifique ( CNRS ), Service d'Endocrinologie, Diabétologie et d'Endocrinologie de la Reproduction [CHU Saint-Antoine], HAL-UPMC, Gestionnaire, Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut de Cardiométabolisme et Nutrition = Institute of Cardiometabolism and Nutrition [CHU Pitié Salpêtrière] (IHU ICAN), CHU Pitié-Salpêtrière [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)-CHU Pitié-Salpêtrière [AP-HP], Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), RIKEN Research Center for Allergy and Immunology, Yokohama (RCAI), Research Unit for Immune Homeostasis, Kobe University, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), and Chadjichristos, Christos

Subjects
0301 basic medicine, Male, Chemokine, Endocrinology, Diabetes and Metabolism, Adipose tissue, Energy homeostasis, Mice, RNA, Small Interfering, Cells, Cultured, 2. Zero hunger, [SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Mice, Knockout, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, biology, Cell Differentiation, [ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Adipose Tissue, Liver, Body Composition, Female, medicine.symptom, medicine.medical_specialty, Adipokine, Inflammation, Diet, High-Fat, Proinflammatory cytokine, 03 medical and health sciences, Nephroblastoma Overexpressed Protein, Insulin resistance, stomatognathic system, Internal medicine, 3T3-L1 Cells, Glucose Intolerance, Internal Medicine, medicine, Animals, Obesity, Pancreas, Cell Proliferation, Macrophages, medicine.disease, Mice, Inbred C57BL, Insulin receptor, 030104 developmental biology, Endocrinology, biology.protein, Insulin Resistance, Energy Metabolism, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience; Identification of new adipokines that potentially link obesity to insulin resistance represents a major challenge. We have recently shown that NOV/CCN3, a multifunctional matricellular protein, is synthesized and secreted by adipose tissue, with plasma levels highly correlated with body mass index. NOV has been previously involved in tissue repair, fibrotic and inflammatory diseases, and cancer. However, its role in energy homeostasis remains unknown. We investigated the metabolic phenotype of NOV-/- mice fed a standard or high fat diet (HFD). Strikingly, the weight of NOV-/- mice was markedly lower than that of WT mice but only on a HFD. This was related to a significant decrease in fat mass associated with an increased proportion of smaller adipocytes and to a higher expression of genes involved in energy expenditure. NOV-/- mice fed a HFD displayed improved glucose tolerance and insulin sensitivity. Interestingly, the absence of NOV was associated with a change in macrophages profile (M1-like to M2-like) and in marked decrease in adipose tissue expression of several proinflammatory cytokines and chemokines and to an enhanced insulin signaling. Conversely, treatment of adipocytes by NOV increased chemokine expression. Altogether, these results show that NOV is a new adipocytokine that could be involved in obesity-associated insulin-resistance.

Published
2016

3. Abstract 384: Nov/ccn3: A Potential Antagonist of Angiotensin Ii Effects in Kidney Disease

Author

Christos Chadjichristos, Pierre-Olivier Marchal, Aurelie Cuinet, Jihane Pakradouni, Julie Toubas, Chantal Kazazian, Claire Calmel, Veronique Leblais, Christos Chatziantoniou, and Céle Martinerie

Subjects
Internal Medicine
Abstract

Progression of chronic kidney disease (CKD) represents a constant challenge for the identification of new therapeutic targets. The NOV/CCN3 matricellular protein, belonging to the CCN (CYR61/CCN1, CTGF/CCN2, NOV/CCN3) family, could represent a new endogenous inhibitor of the fibrotic process that plays a crucial role in tissue damage and regression of renal function. However, the relation between NOV and renal disease remains unclear. Our objective was to study whether alterations in renal NOV expression are involved in the progression of CKD. NOV mRNA expression was significantly induced by 2.5-3 fold at 12-16 weeks in renin-transgenic mice (RenTg), a well established model of AngII-mediated nephropathy, through the Angiotensin receptor 1 (AT 1 R) compared to normotensive control animals (n=7 mice per group, p1 R was also observed in VSMC cultures. Furthermore, infection of these cells with an adenovirus recombinant for NOV strongly repressed in a dose-dependent manner the expression of the Angiotensin Receptor 1 reaching 72 and 78% (p1 R regulatory loop. In subsequent studies the NOV-induced downregulation of AT 1 R was abrogated by integrin β1 specific siRNAs. Thus, NOV can attenuate the deleterious profibrotic effects of AngII during the progression of CKD and may provide a potential therapeutic option against this pathology.

Published
2012

4. NOV/CCN3 impairs muscle cell commitment and differentiation

Author

Catherine Dubois, Frederico Calhabeu, Laurent Schaeffer, Gwenvael Le Dréau, Jérôme E. Lafont, Chantal Kazazian, Maryvonne Laurent, and Cécile Martinerie

Subjects
Biology, MyoD, Immediate-Early Proteins, Mice, Nephroblastoma Overexpressed Protein, stomatognathic system, Genes, Reporter, Insulin-Like Growth Factor II, Basic Helix-Loop-Helix Transcription Factors, Morphogenesis, Myocyte, Animals, Humans, Insulin, HES1, Progenitor cell, Muscle, Skeletal, Myogenin, Cells, Cultured, Cell Proliferation, MyoD Protein, Homeodomain Proteins, Muscle Cells, Receptors, Notch, Myogenesis, Connective Tissue Growth Factor, Cell Differentiation, Cell Biology, bacterial infections and mycoses, Cell biology, Culture Media, Cancer research, Intercellular Signaling Peptides and Proteins, Transcription Factor HES-1, MYF5, Myogenic Regulatory Factor 5, C2C12, Signal Transduction
Abstract

NOV (nephroblastoma overexpressed) is a member of a family of proteins which encodes secreted matrix-associated proteins. NOV is expressed during development in dermomyotome and limb buds, but its functions are still poorly defined. In order to understand the role of NOV in myogenic differentiation, C2C12 cells overexpressing NOV (C2-NOV) were generated. These cells failed to engage into myogenic differentiation, whereas they retained the ability to differentiate into osteoblasts. In differentiating conditions, C2-NOV cells remained proliferative, failed to express differentiation markers and lost their ability to form myotubes. Inhibition of differentiation by NOV was also observed with human primary muscle cells. Further examination of C2-NOV cells revealed a strong downregulation of the myogenic determination genes MyoD and Myf5 and of IGF-II expression. MyoD forced expression in C2-NOV was sufficient to restore differentiation and IGF-II induction whereas 10{sup -6} M insulin treatment had no effects. NOV therefore acts upstream of MyoD and does not affect IGF-II induction and signaling. HES1, a target of Notch, previously proposed to mediate NOV action, was not implicated in the inhibition of differentiation. We propose that NOV is a specific cell fate regulator in the myogenic lineage, acting negatively on key myogenic genes thus controlling the transitionmore » from progenitor cells to myoblasts.« less

Published
2004

Catalog

Books, media, physical & digital resources
See catalog results