ADAMTS-7 Inhibits Re-Endothelialization of Injured Arteries and Promotes Vascular Remodeling Via Cleavage of Thrombospondin-1
نویسندگان
چکیده
Deutsches Herzzentrum München, Klinik für Herzund Kreislauferkrankungen, Technische Universität München, München, Germany; Dept of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China; Cardiovascular Division, Kings College London BHF Centre, London, United Kingdom; Dept of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China; School of Basic Medical Sciences, Tianjin University, Beijing, China; Institut für Physiologie, Universität zu Lübeck, Lübeck, Germany; Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) e.V. (German Center for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, Lübeck, Germany; Institut für Integrative und Experimentelle Genomik, Universität zu Lübeck, Lübeck, Germany; Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) e.V. (German Center for Cardiovascular Research), partner site Munich Heart Alliance (MHA), München, Germany These authors contributed equally to this work. The members of the German Mouse Clinic Consortium are listed in the Supplemental Material
منابع مشابه
ADAMTS-7 inhibits re-endothelialization of injured arteries and promotes vascular remodeling through cleavage of thrombospondin-1.
BACKGROUND ADAMTS-7, a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, was recently identified to be significantly associated genomewide with coronary artery disease. However, the mechanisms that link ADAMTS-7 and coronary artery disease risk remain elusive. We have previously demonstrated that ADAMTS-7 promotes vascular smooth muscle cell migration a...
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The migration of vascular smooth muscle cells (VSMCs) plays an essential role during the development of atherosclerosis and restenosis. Extensive studies have implicated the importance of extracellular matrix (ECM)-degrading proteinases in VSMC migration. A recently described family of proteinases, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTs), is capable of degrading ...
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OBJECTIVE Vascular calcification significantly increases cardiovascular morbidity and mortality. We recently reported that the deficiency of cartilage oligomeric matrix protein (COMP) leads to vascular mineralization. We characterized the COMP-degrading metalloproteinase, a disintegrin and metalloproteinase with thrombospondin motifs-7 (ADAMTS-7). Here, we tested whether ADAMTS-7 facilitates va...
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Hemodialysis vascular access can develop venous neointimal hyperplasia (VNH) causing stenosis. Recent clinical and experimental data has demonstrated that there is increased expression of a disintegrin and metalloproteinase thrombospondin motifs-1 (ADAMTS-1) at site of VNH. The experiments outlined in the present paper were designed to test the hypothesis that targeting of the adventitia of the...
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