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6 results on '"MESH: Osteopontin"'

1. Eosinophilia predicts poor clinical outcomes in recent-onset arthritis: results from the ESPOIR cohort

Author

Dewi Guellec, Gabriel J. Tobón, Morgane Milin, Divi Cornec, Gilles Chiocchia, Alain Saraux, Valérie Devauchelle-Pensec, Olivier Vittecocq, Sandrine Jousse-Joulin, Thierry Marhadour, CHRU Brest - Service de Rhumatologie (CHU - BREST - Rhumato), Centre Hospitalier Régional Universitaire de Brest (CHRU Brest), Lymphocytes B, Autoimmunité et Immunothérapies (LBAI), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-LabEX IGO Immunothérapie Grand Ouest-Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO), Department of Internal Medicine (Dep Med - Div Rheum - CALI), Fundacion Vallee del Lili, Infection et inflammation (2I), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de rhumatologie [CHU Rouen], CHU Rouen, Normandie Université (NU)-Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU), Physiopathologie et biothérapies des maladies inflammatoires et autoimmunes, Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Investigation Clinique [CHU Rouen] (CIC Rouen), Hôpital Charles Nicolle [Rouen]-CHU Rouen, Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Investigation Clinique (CIC - Brest), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM), Lymphocyte B et Auto-immunité (LBAI), and Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Brestois Santé Agro Matière (IBSAM)

Subjects
Pathology, MESH: Osteopontin, Inflammatory arthritis, [SDV]Life Sciences [q-bio], Arthritis, DMARDs (biologic), Early Arthritis, 0302 clinical medicine, Early Rheumatoid Arthritis, Immunology and Allergy, Medicine, Eosinophilia, MESH: Autoantibodies, 0303 health sciences, MESH: Arthritis, Rheumatoid, MESH: Peptides, MESH: Polymorphism, Single Nucleotide, MESH: Genetic Predisposition to Disease, respiratory system, MESH: Case-Control Studies, 3. Good health, medicine.anatomical_structure, [SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system, Rheumatoid arthritis, Cohort, medicine.symptom, DMARDs (synthetic), Cohort study, medicine.medical_specialty, Visual analogue scale, Immunology, Rheumatoid Arthritis, 03 medical and health sciences, Rheumatology, Internal medicine, 030304 developmental biology, 030203 arthritis & rheumatology, MESH: Humans, business.industry, MESH: Alleles, MESH: Macrophages, MESH: Haplotypes, Eosinophil, medicine.disease, MESH: Male, business, MESH: Citrulline, MESH: Female, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Objectives To determine the prevalence of eosinophilia in patients with recent-onset arthritis suggestive of rheumatoid arthritis (RA) and to describe their features and outcomes. Methods We performed an ancillary study of data from a French prospective multicentre cohort study monitoring clinical, laboratory and radiographic data in patients with inflammatory arthritis of 6 weeks to 6 months duration. We determined the proportion of patients with eosinophilia, defined as a count >500/mm3, at baseline and after 3 years. Features of patients with and without baseline eosinophilia were compared. Results Baseline eosinophilia was evidenced in 26 of 804 (3.2%) patients; their mean eosinophil count was 637.7±107/mm3. Baseline eosinophilia was ascribed to atopic syndrome in 6 of 26 (23.1%) patients. After 3 years, patients with eosinophilia had higher Health Assessment Questionnaire scores (0.9 vs 0.5, p=0.004), higher patient visual analogue scale activity score and morning stiffness intensity (p=0.05), and were more often taking disease-modifying antirheumatic drugs (p=0.02). Baseline eosinophilia was not associated with presence of extra-articular manifestations. Conclusions Eosinophilia is rare in recent-onset arthritis suggestive of RA, and is usually directly related to the rheumatic disease. Our data suggest that patients with mild eosinophilia at diagnosis could respond worse to the treatment than those without.

Published
2015
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2. SPP1 rs9138 variant contributes to the severity of radiological damage in anti-citrullinated protein autoantibody-negative rheumatoid arthritis

Author

Gabriel J. Tobón, Thierry Schaeverbeke, Philippe Dieudé, Steven Gazal, Valérie Devauchelle-Pensec, Pierre-Antoine Juge, Hanna W. van Steenbergen, Bernard Combe, Arnaud Constantin, Annette H M van der Helm-van Mil, Delphine Nigon, Biologie de l'Os et du Cartilage : Régulations et Ciblages Thérapeutiques (BIOSCAR (UMR_S_1132 / U1132)), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of rheumatology, Leiden University Medical Center (LUMC), Epidémiologie et analyses en santé publique : risques, maladies chroniques et handicaps (LEASP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Immunologie et Pathologie (EA2216), Université de Brest (UBO)-IFR148, Université Paris Diderot - Paris 7 (UPD7), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC), Département de Rhumatologie[Montpellier], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Lapeyronie, Centre d'Investigation Clinique (CIC - Brest), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM), Lymphocyte B et Auto-immunité (LBAI), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO), CHRU Brest - Service de Rhumatologie (CHU - BREST - Rhumato), Centre Hospitalier Régional Universitaire de Brest (CHRU Brest), Service de rhumatologie, Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse], Department of Rheumatology, Service de rhumatologie [Bichat], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), 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), Centre d'Investigation Clinique INSERM 1412 (CIC 1412 - BREST), Mécanismes, Conséquences et Modulation de l'Inflammation Ostéo-articulaire, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris]-Université Paris Diderot - Paris 7 (UPD7), and Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Oncology, Male, Pathology, MESH: Osteopontin, [SDV]Life Sciences [q-bio], Arthritis, Rheumatoid, MESH: Genotype, 0302 clinical medicine, Early Rheumatoid Arthritis, Immunology and Allergy, MESH: Autoantibodies, MESH: Genetic Variation, MESH: Radiography, MESH: Aged, 0303 health sciences, education.field_of_study, MESH: Arthritis, Rheumatoid, MESH: Middle Aged, MESH: Genetic Predisposition to Disease, Middle Aged, Connective tissue disease, MESH: Case-Control Studies, [SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system, Rheumatoid arthritis, Cohort, Disease Progression, Female, MESH: Disease Progression, Adult, musculoskeletal diseases, medicine.medical_specialty, MESH: Hand Joints, Genotype, Hand Joints, Immunology, Population, Rheumatoid Arthritis, Peptides, Cyclic, General Biochemistry, Genetics and Molecular Biology, MESH: Foot Joints, 03 medical and health sciences, Rheumatology, Gene Polymorphism, Internal medicine, Foot Joints, medicine, Humans, Genetic Predisposition to Disease, education, Genotyping, MESH: Peptides, Cyclic, 030304 developmental biology, Aged, Autoantibodies, 030203 arthritis & rheumatology, MESH: Humans, business.industry, Autoantibody, Genetic Variation, MESH: Adult, medicine.disease, MESH: Male, Minor allele frequency, Radiography, Case-Control Studies, Ant-CCP, Osteopontin, Gene polymorphism, business, MESH: Female, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Objective We recently reported an association of the SPP1 rs9138 and rs11439060 functional variants with the risk of rheumatoid arthritis (RA), the association being greater in anti-citrullinated protein autoantibody (ACPA)-negative patients. We hypothesised that SPP1 may contribute to the severity of joint destruction in RA, specifically in the ACPA-negative population. Methods Patients with RA in the ESPOIR cohort underwent genotyping for SPP1 rs9138 and rs11439060. Radiographs of the hands and feet were obtained at the first visit and at 1- and 2-year follow-up. Association analyses were performed by ACPA status. A replication study of the relevant subset of the Leiden Early Arthritis Clinic (EAC) cohort was performed. Results In the ESPOIR cohort (652 patients), rs9138 was significantly associated with radiological progression of joint destruction at 2 years, the association being restricted to 358 ACPA-negative patients (p=0.034). In the replication study with the Leiden EAC cohort (273 ACPA-negative patients), rs4754, which is in complete linkage disequilibrium with rs9138, was significantly associated with joint damage progression in ACPA-negative patients at 2- and 7-year follow-up (p=0.019 and p=0.005, respectively). Combined analysis of the two cohorts revealed a 0.95-fold rate of joint destruction per year per minor allele (p=0.022). Conclusions The SPP1 rs9138 variant contributes to joint damage progression in ACPA-negative RA.

Published
2014

3. Osteopontin expression in cardiomyocytes induces dilated cardiomyopathy

Author

Patricia Reant, Fanny Robbesyn, Thierry Couffinhal, Flavien Charpentier, Karin Klingel, Danièle Daret, Claude Desgranges, Cécile Allières, Victorine Douin, Marie-Ange Renault, Isabelle Belloc, Pierre Dos Santos, Jean-François Arnal, Alain-Pierre Gadeau, Simon, Marie Francoise, Adaptation cardiovasculaire à l'ischemie, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Bordeaux Segalen - Bordeaux 2, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Molecular Pathology, Institute for Pathology-Universitary Hospital of Tubingen, Institut du thorax, Université de Nantes (UN)-IFR26-Institut National de la Santé et de la Recherche Médicale (INSERM), Cardiopathies et mort subite [ERL 3147], Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Heart disease, MESH: Osteopontin, Cardiomyopathy, MESH: Myocytes, Cardiac, 030204 cardiovascular system & hematology, Lymphocyte Activation, Mice, 0302 clinical medicine, Myocyte, Myocytes, Cardiac, MESH: Animals, Osteopontin, 0303 health sciences, biology, Dilated cardiomyopathy, 3. Good health, Myocarditis, Neutrophil Infiltration, MESH: Fibrosis, medicine.symptom, Cardiology and Cardiovascular Medicine, Cardiomyopathy, Dilated, medicine.medical_specialty, MESH: Mice, Transgenic, Mice, Transgenic, Inflammation, 03 medical and health sciences, stomatognathic system, MESH: Myocarditis, Internal medicine, medicine, Animals, MESH: Cardiomyopathy, Dilated, MESH: Lymphocyte Activation, MESH: Mice, 030304 developmental biology, Heart Failure, business.industry, medicine.disease, Fibrosis, Disease Models, Animal, MESH: Neutrophil Infiltration, Endocrinology, Heart failure, MESH: Heart Failure, biology.protein, MESH: Disease Models, Animal, business
Abstract

Background— Inflammatory processes play a critical role in myocarditis, dilated cardiomyopathy, and heart failure. The expression of the inflammatory chemokine osteopontin (OPN) is dramatically increased in cardiomyocytes and inflammatory cells during myocarditis and heart failure in human and animals. However, its role in the development of heart diseases is not known. Methods and Results— To understand whether OPN is involved in cardiomyopathies, we generated a transgenic mouse (MHC-OPN) that specifically overexpresses OPN in cardiomyocytes with cardiac-specific promoter-directed OPN expression. Young MHC-OPN mice were phenotypically indistinguishable from their control littermates, but most of them died prematurely with a half-life of 12 weeks of age. Electrocardiography revealed conduction defects. Echocardiography showed left ventricular dilation and systolic dysfunction. Histological analysis revealed cardiomyocyte loss, severe fibrosis, and inflammatory cell infiltration. Most of these inflammatory cells were activated T cells with Th1 polarization and cytotoxic activity. Autoantibodies against OPN, cardiac myosin, or troponin I, were not found in the serum of MHC-OPN mice. Conclusions— These data show that OPN expression in the heart induces in vivo T-cell recruitment and activation leading to chronic myocarditis, the consequence of which is myocyte destruction and hence, dilated cardiomyopathy. Thus, OPN might therefore constitute a potential therapeutic target to limit heart failure.

Published
2010
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4. Elevated expression of osteopontin may be related to adipose tissue macrophage accumulation and liver steatosis in morbid obesity

Author

Adeline Bertola, Keith N. Frayn, Yannick Le Marchand-Brustel, Joan Tordjman, Moncef Dahman, S. McQuaid, Albert Tran, Philippe Gual, Karine Clément, Vanessa Deveaux, Jean Gugenheim, Pierre-Michel Huet, Rodolphe Anty, Déborah Rousseau, Sophie Lotersztajn, Abdelilah Wakkach, Stéphanie Bonnafous, Centre méditérannéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), 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, Signalisation moléculaire et obésité, COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM), Transduction du Signal : Signalisation Calcique et Phosphorylation, Université Joseph Fourier - Grenoble 1 (UJF)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Génétique, physiopathologie et ingénierie du tissu osseux (GéPITOS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Paris Descartes - Paris 5 (UPD5)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), University of Oxford [Oxford], Environnement et Grandes Cultures (EGC), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, Service de Chirurgie Digestive et Transplantation Hépatique, Hôpital Archet II, Digestive Center, Centre Hospitalier Universitaire de Nice (CHU Nice), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Centre National de la Recherche Scientifique (CNRS), 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)-Centre National de la Recherche Scientifique (CNRS), AgroParisTech-Institut National de la Recherche Agronomique (INRA), Centre méditérannéen de médecine moléculaire ( C3M ), Université Nice Sophia Antipolis ( UNS ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut Mondor de Recherche Biomédicale ( IMRB ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -IFR50-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Joseph Fourier - Grenoble 1 ( UJF ) -Commissariat à l'énergie atomique et aux énergies alternatives ( CEA ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Génétique, physiopathologie et ingénierie du tissu osseux ( GéPITOS ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Centre National de la Recherche Scientifique ( CNRS ), Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), 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 ) -Centre National de la Recherche Scientifique ( CNRS ), Oxford Centre for Diabetes, Endocrinology and Metabolism ( OCDEM ), Environnement et Grandes Cultures ( EGC ), AgroParisTech-Institut National de la Recherche Agronomique ( INRA ), Epidémiologie et écologie des maladies animales ( Epidémiologie ), Centre de Coopération Internationale en Recherche Agronomique pour le Développement ( CIRAD ), CHU Nice, Université Nice Sophia Antipolis (1965 - 2019) (UNS), University of Oxford, and Service de Chirurgie Digestive / Centre de Transplantation Hépatique [CHU Nice]

Subjects
Male, MESH : RNA, Messenger, Endocrinology, Diabetes and Metabolism, Mice, 0302 clinical medicine, MESH : Oleic Acid, MESH: Animals, Osteopontin, MESH : Immunoblotting, MESH : Macrophages, Liver injury, 0303 health sciences, Tumor, MESH: Middle Aged, MESH: Immunoblotting, MESH : Reverse Transcriptase Polymerase Chain Reaction, Obesity, Morbid, Hyaluronan Receptors, Adipose Tissue, Tumor necrosis factor alpha, MESH: Adipose Tissue, medicine.medical_specialty, MESH: Gene Expression, MESH: Antigens, CD44, MESH : Adipose Tissue, 03 medical and health sciences, MESH: Weight Loss, Humans, MESH : Middle Aged, RNA, Messenger, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Humans, Tumor Necrosis Factor-alpha, Macrophages, MESH : Humans, MESH: Oleic Acid, MESH: Adult, medicine.disease, Mice, Inbred C57BL, MESH : Gene Expression, Endocrinology, MESH: Tumor Necrosis Factor-alpha, MESH: Female, MESH: Liver, MESH : Fatty Liver, MESH: Osteopontin, Messenger, Adipose tissue, Gene Expression, Inbred C57BL, MESH: Reverse Transcriptase Polymerase Chain Reaction, MESH : Antigens, CD44, MESH : Female, MESH : Osteopontin, CD44, Morbid, Receptor, MESH: Fatty Liver, MESH : Tumor Necrosis Factor-alpha, biology, Reverse Transcriptase Polymerase Chain Reaction, Fatty liver, MESH : Adult, Middle Aged, Liver, Female, Obesity Studies, Adult, MESH : Obesity, Morbid, MESH: Cell Line, Tumor, MESH : Male, Immunoblotting, 030209 endocrinology & metabolism, MESH : Mice, Inbred C57BL, Cell Line, Insulin resistance, stomatognathic system, MESH: Mice, Inbred C57BL, Cell Line, Tumor, Internal medicine, MESH : Mice, Weight Loss, Internal Medicine, medicine, Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Obesity, Antigens, MESH: Mice, 030304 developmental biology, MESH: RNA, Messenger, MESH : Cell Line, Tumor, MESH : Liver, MESH: Macrophages, MESH: Obesity, Morbid, MESH: Male, Fatty Liver, biology.protein, RNA, MESH : Animals, MESH : Weight Loss, Steatosis, Oleic Acid
Abstract

OBJECTIVE—Osteopontin (OPN) plays an important role in the development of insulin resistance and liver complications in dietary murine models. We aimed to determine the expression pattern of OPN and its receptor CD44 in obese patients and mice according to insulin resistance and liver steatosis. RESEARCH DESIGN AND METHODS—OPN and CD44 expressions were studied in 52 morbidly obese patients and in mice. Cellular studies were performed in HepG2 cells. RESULTS—Hepatic OPN and CD44 expressions were strongly correlated with liver steatosis and insulin resistance in obese patients and mice. This increased OPN expression could be due to the accumulation of triglycerides, since fat loading in HepG2 promotes OPN expression. In contrast, OPN expression in adipose tissue (AT) was enhanced independently of insulin resistance and hepatic steatosis in obese patients. The elevated OPN expression in AT was paralleled with the AT macrophage infiltration, and both phenomena were reversed after weight loss. The circulating OPN level was slightly elevated in obese patients and was not related to liver steatosis. Further, AT did not appear to secrete OPN. In contrast, bariatric surgery–induced weight loss induced a strong increase in circulating OPN. CONCLUSIONS—The modestly elevated circulating OPN levels in morbidly obese patients were not related to liver steatosis and did not appear to result from adipose tissue secretion. In subcutaneous AT, expression of OPN was directly related to macrophage accumulation independently from liver complications. In contrast, hepatic OPN and CD44 expressions were related to insulin resistance and steatosis, suggesting their local implication in the progression of liver injury.

Published
2009
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5. Preventive effects of nutritional doses of polyphenolic molecules on cardiac fibrosis associated with metabolic syndrome: involvement of osteopontin and oxidative stress

Author

Jacqueline Azay-Milhau, Gérard Cros, Pierre-Louis Teissedre, Thibault Sutra, E. Youl, Jean-Paul Cristol, R. Magous, Catherine Oiry, Centre de pharmacologie et innovation dans le diabète (CPID), Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Centre National de la Recherche Scientifique (CNRS), and Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Université Montpellier 1 (UM1)

Subjects
Cardiac fibrosis, MESH: Osteopontin, MESH: Collagen Type I, MESH: Rats, Sprague-Dawley, 030204 cardiovascular system & hematology, Resveratrol, medicine.disease_cause, Rats, Sprague-Dawley, chemistry.chemical_compound, 0302 clinical medicine, MESH: Phenols, Fibrosis, MESH: Animals, Gallic acid, Osteopontin, chemistry.chemical_classification, 0303 health sciences, MESH: Oxidative Stress, biology, MESH: Heart Diseases, food and beverages, MESH: Reactive Oxygen Species, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, 3. Good health, MESH: Insulin Resistance, MESH: Fibrosis, Delphinidin, General Agricultural and Biological Sciences, medicine.medical_specialty, Heart Diseases, MESH: Rats, Collagen Type I, 03 medical and health sciences, Phenols, Internal medicine, medicine, Animals, Humans, 030304 developmental biology, Flavonoids, Reactive oxygen species, MESH: Humans, Polyphenols, General Chemistry, medicine.disease, Rats, Oxidative Stress, Endocrinology, chemistry, biology.protein, Insulin Resistance, Reactive Oxygen Species, MESH: Flavonoids, Oxidative stress
Abstract

International audience; We previously showed that grape extracts enriched in different polyphenolic families were similarly able to prevent reactive oxygen species (ROS) production, although having differential effects on various features of metabolic syndrome when administered at a dose of 21 mg/kg to the fructose (60%)-fed rat (a model of metabolic syndrome). In the present work, we analyzed on the same model the effect of pure polyphenolic molecules (catechin, resveratrol, delphinidin, and gallic acid) administered at a dose of 2.1 mg/kg. Delphinidin and gallic acid prevented insulin resistance, while gallic acid prevented the elevation of blood pressure. All molecules prevented cardiac ROS overproduction and NADPH overexpression. We also showed that fructose feeding was associated with cardiac fibrosis (accumulation of collagen I) and expression of osteopontin, a factor induced by ROS and a collagen I expression inducer. Collagen I and osteopontin expressions were prevented by the administration of all polyphenolic molecules. The potential use of polyphenols in the prevention of cardiac fibrosis should be further explored.

Published
2008
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6. Paracrine and Autocrine Signals Promoting Full Chondrogenic Differentiation of a Mesoblastic Cell Line

Author

Michel Huerre, Odile Kellermann, Marie Boucquey, Huot Khun, Morgane Locker, Anne Poliard, Génétique moléculaire et intégration des fonctions cellulaires (GMIFC), Centre National de la Recherche Scientifique (CNRS), Brussels Branch and Cellular Genetics Unit, Ludwig Institute for Cancer Research, and Unité d'Anatomo-pathologie, Institut Pasteur

Subjects
MESH: Extracellular Matrix Proteins, MESH: Signal Transduction, MESH: Osteopontin, Endocrinology, Diabetes and Metabolism, Cellular differentiation, MESH: Bone Morphogenetic Proteins, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, MESH: Insulin-Like Growth Factor I, MESH: Collagen Type I, SMAD, MESH: Triiodothyronine, Culture Media, Serum-Free, Dexamethasone, Mice, MESH: Transforming Growth Factor beta1, 0302 clinical medicine, MESH: Cell Aggregation, MESH: Aggrecans, Transforming Growth Factor beta, MESH: Reverse Transcriptase Polymerase Chain Reaction, MESH: Up-Regulation, Orthopedics and Sports Medicine, MESH: Animals, Aggrecans, Insulin-Like Growth Factor I, MESH: Sialoglycoproteins, BMP signaling pathway, Cell Aggregation, MESH: Collagen Type X, Extracellular Matrix Proteins, 0303 health sciences, [SDV.NEU.PC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior, Reverse Transcriptase Polymerase Chain Reaction, High Mobility Group Proteins, [SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences, Cell Differentiation, SOX9 Transcription Factor, MESH: Gene Expression Regulation, Neoplastic, MESH: Transcription Factors, MESH: Culture Media, Serum-Free, Immunohistochemistry, Up-Regulation, Cell biology, Gene Expression Regulation, Neoplastic, Autocrine Communication, medicine.anatomical_structure, 030220 oncology & carcinogenesis, MESH: Dexamethasone, MESH: Proteoglycans, Bone Morphogenetic Proteins, Triiodothyronine, MESH: Pluripotent Stem Cells, Proteoglycans, Signal Transduction, Pluripotent Stem Cells, MESH: Cell Differentiation, medicine.medical_specialty, MESH: Cell Line, Tumor, Sialoglycoproteins, Biology, Bone morphogenetic protein, MESH: Bone Morphogenetic Protein Receptors, Collagen Type I, Chondrocyte, Transforming Growth Factor beta1, 03 medical and health sciences, Paracrine signalling, MESH: SOX9 Transcription Factor, Chondrocytes, Cell Line, Tumor, Internal medicine, MESH: Chondrocytes, Paracrine Communication, MESH: Receptors, Growth Factor, medicine, Animals, MESH: Blotting, Northern, Lectins, C-Type, Receptors, Growth Factor, MESH: Paracrine Communication, Autocrine signalling, Collagen Type II, MESH: Mice, MESH: Transforming Growth Factor beta, 030304 developmental biology, MESH: Immunohistochemistry, Bone Morphogenetic Protein Receptors, MESH: Collagen Type II, Blotting, Northern, Chondrogenesis, MESH: High Mobility Group Proteins, Endocrinology, Osteopontin, MESH: Autocrine Communication, MESH: Lectins, C-Type, Collagen Type X, Transcription Factors
Abstract

The pluripotent mesoblastic C1 cell line was used under serum-free culture conditions to investigate how paracrine and autocrine signals cooperate to drive chondrogenesis. Sequential addition of two systemic hormones, dexamethasone and triiodothyronine, permits full chondrogenic differentiation. The cell intrinsic activation of the BMP signaling pathway and Sox9 expression occurring on mesoblastic condensation is insufficient for recruitment of the progenitors. Dexamethasone-dependent Sox9 upregulation is essential for chondrogenesis. Introduction: Differentiation of lineage stem cells relies on cell autonomous regulations modulated by external signals. We used the pluripotent mesoblastic C1 cell line under serum-free culture conditions to investigate how paracrine and autocrine signals cooperate to induce differentiation of a precursor clone along the chondrogenic lineage. Materials and Methods: C1 cells, cultured as aggregates, were induced toward chondrogenesis by addition of 10−7 M dexamethasone in serum-free medium. After 30 days, dexamethasone was replaced by 10 nM triiodothyronine to promote final hypertrophic conversion. Mature and hypertrophic phenotypes were characterized by immunocytochemistry using specific antibodies against types II and X collagens, respectively. Type II collagen, bone morphogenetic proteins (BMPs), BMP receptors, Smads, and Sox9 expression were monitored by reverse transcriptase-polymerase chain reaction (RT-PCR), Northern blot, and/or Western blot analysis. Results and Conclusions: Once C1 cells have formed nodules, sequential addition of two systemic hormones is sufficient to promote full chondrogenic differentiation. In response to dexamethasone, nearly 100% of the C1 precursors engage in chondrogenesis and convert within 30 days into mature chondrocytes, which triggers a typical cartilage matrix. On day 25, a switch in type II procollagen mRNA splicing acted as a limiting step in the acquisition of the mature chondrocyte phenotype. On day 30, substitution of dexamethasone with triiodothyronine triggers the final differentiation into hypertrophic chondrocytes within a further 15 days. The chondrogenic process is supported by intrinsic expression of Sox9 and BMP family genes. Similarly to the in vivo situation, activation of Sox9 expression and the BMP signaling pathway occurred on mesoblastic condensation. After induction, BMP-activated Smad nuclear translocation persisted throughout the process until the onset of hypertrophy. After dexamethasone addition, Sox9 expression was upregulated. Dexamethasone withdrawal reversed the increase in Sox9 expression and stopped differentiation. Thus, Sox9 seems to be a downstream mediator of dexamethasone action.

Published
2004
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