ADAMTS-7 promotes vascular smooth muscle cells proliferation in vitro and in vivo

[1]  Shi-You Chen,et al.  Mechanisms simultaneously regulate smooth muscle proliferation and differentiation , 2013, Journal of biomedical research.

[2]  M. Caulfield,et al.  ADAMTS7 cleavage and vascular smooth muscle cell migration is affected by a coronary-artery-disease-associated variant. , 2013, American journal of human genetics.

[3]  Qingbo Xu,et al.  Upregulation of a Disintegrin and Metalloproteinase With Thrombospondin Motifs-7 by miR-29 Repression Mediates Vascular Smooth Muscle Calcification , 2012, Arteriosclerosis, thrombosis, and vascular biology.

[4]  Jean-Baptiste Michel,et al.  The vascular smooth muscle cell in arterial pathology: a cell that can take on multiple roles. , 2012, Cardiovascular research.

[5]  A. Didangelos,et al.  Novel Role of ADAMTS-5 Protein in Proteoglycan Turnover and Lipoprotein Retention in Atherosclerosis* , 2012, The Journal of Biological Chemistry.

[6]  N. Mehta.  Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease. , 2011, Circulation. Cardiovascular genetics.

[7]  Qingbo Xu,et al.  Cartilage Oligomeric Matrix Protein Inhibits Vascular Smooth Muscle Calcification by Interacting With Bone Morphogenetic Protein-2 , 2011, Circulation research.

[8]  Mark I. McCarthy,et al.  A genome-wide association study in Europeans and South Asians identifies five new loci for coronary artery disease , 2011, Nature Genetics.

[9]  T. Assimes,et al.  Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies , 2011, The Lancet.

[10]  D. Ramji,et al.  ADAMTS proteases: key roles in atherosclerosis? , 2010, Journal of Molecular Medicine.

[11]  Qingbo Xu,et al.  Cartilage Oligomeric Matrix Protein Maintains the Contractile Phenotype of Vascular Smooth Muscle Cells by Interacting With &agr;7&bgr;1 Integrin , 2010, Circulation research.

[12]  S. Apte.  A Disintegrin-like and Metalloprotease (Reprolysin-type) with Thrombospondin Type 1 Motif (ADAMTS) Superfamily: Functions and Mechanisms* , 2009, The Journal of Biological Chemistry.

[13]  S. Hollenbeck,et al.  TGF-beta through Smad3 signaling stimulates vascular smooth muscle cell proliferation and neointimal formation. , 2009, American journal of physiology. Heart and circulatory physiology.

[14]  Bo Liu,et al.  ADAMTS-7 Mediates Vascular Smooth Muscle Cell Migration and Neointima Formation in Balloon-Injured Rat Arteries , 2009, Circulation research.

[15]  J. Foidart,et al.  ADAMTS-1 metalloproteinase promotes tumor development through the induction of a stromal reaction in vivo. , 2008, Cancer research.

[16]  M. Pfeffer,et al.  Association Between ADAMTS1 Matrix Metalloproteinase Gene Variation, Coronary Heart Disease, and Benefit of Statin Therapy , 2008, Arteriosclerosis, thrombosis, and vascular biology.

[17]  Hanna Björk,et al.  ADAMTS-4 and -8 are inflammatory regulated enzymes expressed in macrophage-rich areas of human atherosclerotic plaques. , 2008, Atherosclerosis.

[18]  Jialiang Hu,et al.  Matrix metalloproteinase inhibitors as therapy for inflammatory and vascular diseases , 2007, Nature Reviews Drug Discovery.

[19]  Achmad Rudijanto,et al.  The role of vascular smooth muscle cells on the pathogenesis of atherosclerosis. , 2007, Acta medica Indonesiana.

[20]  W. Kong,et al.  ADAMTS‐7: a metalloproteinase that directly binds to and degrades cartilage oligomeric matrix protein , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[21]  A. Newby,et al.  Matrix metalloproteinases regulate migration, proliferation, and death of vascular smooth muscle cells by degrading matrix and non-matrix substrates. , 2006, Cardiovascular research.

[22]  J. Sluijter,et al.  Vascular Remodeling and Protease Inhibition—bench to Bedside , 2022 .

[23]  Jian-Mei Li,et al.  Aldosterone and Angiotensin II Synergistically Induce Mitogenic Response in Vascular Smooth Muscle Cells , 2005, Circulation research.

[24]  A. Fourie,et al.  ADAMTS5 is the major aggrecanase in mouse cartilage in vivo and in vitro , 2005, Nature.

[25]  R. Fritsche-Danielson,et al.  Role of ADAMTS-1 in Atherosclerosis: Remodeling of Carotid Artery, Immunohistochemistry, and Proteolysis of Versican , 2004 .

[26]  R. Fritsche-Danielson,et al.  Role of ADAMTS-1 in atherosclerosis: remodeling of carotid artery, immunohistochemistry, and proteolysis of versican. , 2004, Arteriosclerosis, thrombosis, and vascular biology.

[27]  D. Courtman,et al.  A nonantibiotic chemically modified tetracycline (CMT-3) inhibits intimal thickening. , 2003, The American journal of pathology.

[28]  Giulio Gabbiani,et al.  Arterial Smooth Muscle Cell Heterogeneity: Implications for Atherosclerosis and Restenosis Development , 2003, Arteriosclerosis, thrombosis, and vascular biology.

[29]  M. Iruela-Arispe,et al.  ADAMTS1/METH1 Inhibits Endothelial Cell Proliferation by Direct Binding and Sequestration of VEGF165* , 2003, Journal of Biological Chemistry.

[30]  A. Cho,et al.  Matrix Metalloproteinase-9 Is Necessary for the Regulation of Smooth Muscle Cell Replication and Migration After Arterial Injury , 2002, Circulation research.

[31]  Z. Galis,et al.  Targeted Disruption of the Matrix Metalloproteinase-9 Gene Impairs Smooth Muscle Cell Migration and Geometrical Arterial Remodeling , 2002, Circulation research.

[32]  B. Strauss,et al.  Doxycycline modulates smooth muscle cell growth, migration, and matrix remodeling after arterial injury. , 2002, The American journal of pathology.

[33]  A. Koff,et al.  Cell-cycle inhibitors: three families united by a common cause. , 2000, Gene.

[34]  R. Wynn,et al.  Purification and cloning of aggrecanase-1: a member of the ADAMTS family of proteins. , 1999, Science.

[35]  S. Elledge,et al.  How the Cyclin Became a Cyclin Regulated Proteolysis in the Cell Cycle , 1999, Cell.

[36]  B. Lämmle,et al.  Acquired deficiency of von Willebrand factor-cleaving protease in a patient with thrombotic thrombocytopenic purpura. , 1998, Blood.

[37]  Stephen J. Elledge,et al.  Cell Cycle Checkpoints: Preventing an Identity Crisis , 1996, Science.

[38]  C. Pepine,et al.  Localization of insulin-like growth factor I and inhibition of coronary smooth muscle cell growth by somatostatin analogues in human coronary smooth muscle cells. A potential treatment for restenosis? , 1994, Circulation.

[39]  J. Rapp.  Inhibition of neointimal smooth muscle accumulation after angioplasty by an antibody to PDGF , 1993 .

[40]  M. Reidy,et al.  Proliferation of smooth muscle cells after vascular injury is inhibited by an antibody against basic fibroblast growth factor. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[41]  S. Slater,et al.  MMP-9 and -12 cause N-cadherin shedding and thereby beta-catenin signalling and vascular smooth muscle cell proliferation. , 2009, Cardiovascular research.

[42]  H. Ma,et al.  Deletion of active ADAMTS5 prevents cartilage degradation in a murine model of osteoarthritis , 2007, Nature.

[43]  M. Iruela-Arispe,et al.  ADAMTS 1 / METH 1 Inhibits Endothelial Cell Proliferation by Direct Binding and Sequestration of VEGF 165 * , 2003 .