Prokineticin receptor-1 induces neovascularization and epicardial-derived progenitor cell differentiation

التفاصيل البيبلوغرافية
العنوان: Prokineticin receptor-1 induces neovascularization and epicardial-derived progenitor cell differentiation
المؤلفون: Nadia Messaddeq, Canan G. Nebigil, Kyoji Urayama, Selçuk Takır, Hitoshi Kurose, Célia Guilini, Gulen Turkeri, Andrée Dierich
المساهمون: Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Clinique de la Souris (ICS), Intégrité du génome, Ecole Supérieure de Biotechnologie de Strasbourg (ESBS), Université de Strasbourg (UNISTRA)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Laboratoire des biomolécules (LBM UMR 7203), Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Département de Chimie - ENS Paris, École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Chimie Moléculaire de Paris Centre (FR 2769), Institut de Chimie du CNRS (INC)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-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)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Louis Pasteur - Strasbourg I
المصدر: Arteriosclerosis, Thrombosis, and Vascular Biology
Arteriosclerosis, Thrombosis, and Vascular Biology, American Heart Association, 2008, 28 (5), pp.841-9. ⟨10.1161/ATVBAHA.108.162404⟩
Arteriosclerosis, Thrombosis, and Vascular Biology, American Heart Association, 2008, 28 (5), pp.841-849. ⟨10.1161/ATVBAHA.108.162404⟩
بيانات النشر: HAL CCSD, 2008.
سنة النشر: 2008
مصطلحات موضوعية: MESH: Signal Transduction, MESH: Pericardium, Angiogenesis, Cellular differentiation, MESH: Myocytes, Cardiac, 030204 cardiovascular system & hematology, MESH: Neuropeptides, Muscle, Smooth, Vascular, Mice, 0302 clinical medicine, Cell Movement, MESH: Up-Regulation, Myocytes, Cardiac, MESH: Animals, MESH: Gastrointestinal Hormones, MESH: Cell Movement, Protein Kinase C, ComputingMilieux_MISCELLANEOUS, 0303 health sciences, Stem Cells, Cell Differentiation, MESH: Muscle, Smooth, Vascular, Prokineticin, Cell biology, Up-Regulation, MESH: Endothelium, Vascular, Cardiology and Cardiovascular Medicine, Pericardium, MESH: Neovascularization, Physiologic, Signal Transduction, MESH: Cell Differentiation, medicine.medical_specialty, MESH: Mice, Transgenic, Transgene, Neovascularization, Physiologic, Mice, Transgenic, MESH: Stem Cells, Biology, Gastrointestinal Hormones, MESH: Coculture Techniques, 03 medical and health sciences, Paracrine signalling, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Internal medicine, MESH: Cell Proliferation, medicine, Animals, Progenitor cell, Autocrine signalling, MESH: Mice, 030304 developmental biology, Cell Proliferation, Neuropeptides, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, Prokineticin receptor 1, MESH: Protein Kinase C, Coculture Techniques, Endocrinology, Endothelium, Vascular
الوصف: Objective— Identification of novel factors that contribute to myocardial repair and collateral vessel growth hold promise for treatment of heart diseases. We have shown that transient prokineticin receptor-1 (PKR1) gene transfer protects the heart against myocardial infarction in a mouse model. Here, we investigated the role of excessive PKR1 signaling in heart. Methods and Results— Transgenic mice overexpressing PKR1 in cardiomyocytes displayed no spontaneous abnormalities in cardiomyocytes but showed an increased number of epicardial-derived progenitor cells (EPDCs), capillary density, and coronary arterioles. Coculturing EPDCs with H9c2 cardiomyoblasts overexpressing PKR1 promotes EPDC differentiation into endothelial and smooth muscle cells, mimicking our transgenic model. Overexpressing PKR1 in H9c2 cardiomyoblasts or in transgenic hearts upregulated prokineticin-2 levels. Exogenous prokineticin-2 induces significant outgrowth from neonatal and adult epicardial explants, promoting EPDC differentiation. These prokineticin-2 effects were abolished in cardiac explants from mice with PKR1-null mutation. Reduced capillary density and prokineticin-2 levels in PKR1-null mutant hearts supports the hypothesis of an autocrine/paracrine loop between PKR1 and prokineticin-2. Conclusion— Cardiomyocyte-PKR1 signaling upregulates its own ligand prokineticin-2 that acts as a paracrine factor, triggering EPDCs proliferation/differentiation. This study provides a novel insight for possible therapeutic strategies aiming at restoring pluripotency of adult EPDCs to promote neovasculogenesis by induction of cardiomyocyte PKR1 signaling.
اللغة: English
تدمد: 1079-5642
1524-4636
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3a66360a520d3842486709223df910c0Test
https://hal.archives-ouvertes.fr/hal-00282980Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....3a66360a520d3842486709223df910c0
قاعدة البيانات: OpenAIRE