ADAMTS-7 Mediates Vascular Smooth Muscle Cell Migration and Neointima Formation in Balloon-Injured Rat Arteries

By Li Wang, Jingang Zheng, X. Bai, Bo Liu, Chuan-ju Liu, Qingbo Xu, Yi Zhu, Nanping Wang, W. Kong, Xian Wang. 2009

219 citations recorded by the source corpus.

Subfields: Biomaterials, Cancer Research, Molecular Biology

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Citations in the corpus

• A Disintegrin and Metalloproteinase (ADAM) and ADAM with Thrombospondin Motifs (ADAMTS) Family in Vascular Biology and Disease (2019, background): “ADAMTS-7 mediates VSM cell migration and neointima formation in balloon-injured rat arteries [122].”
• ADAMTS proteins in human disorders (2018, result): “localization to smooth muscle cells, but not macrophages in the lesion, and pinpointed its localization to their cell surface and filopodia [37], consistent with the demonstrated effect of ADAMTS7 in facilitating SMC migration in vitro [79].”
• ADAMTS-7 Inhibits Re-endothelialization of Injured Arteries and Promotes Vascular Remodeling Through Cleavage of Thrombospondin-1 (2015, background): “ADAMTS-7, via he degradation of COMP, promotes neointima formation and vascular calcification.(10,17) Among other potential substrates, we have identified TSP-1 as another ADAMTS-7 target with profound functional implications on endothelial biology following injury.”
• Association between plasma ADAMTS-7 levels and severity of disease in patients with stable obstructive coronary artery disease (2016, background): “Possible mechanisms include: elevated circulation ADAMTS-7 may impair endothelial function by inhibiting endothelial cell proliferation and migration,([20]) meanwhile promote plaque progression by accelerating vascular smooth muscle cell migration,([19]) which results in accelerating the severity of”
• A genome-wide association study in Europeans and South Asians identifies five new loci for coronary artery disease (2011, unknown): “ADAMTS7 is a metalloproteinase that accumulates in carotid artery neointima after injury and is upregulated by platelet-derived growth facto”
• Association between plasma ADAMTS-7 levels and ventricular remodeling in patients with acute myocardial infarction (2015, unknown): “Abbreviations 95% CI: 95% confidence intervals; AMI: acute myocardial infarction; BMI: body mass index; BNP: brain natriuretic peptide; COMP: cartilage oligomeric matrix proteins; ECM: extracellular matrix; ELISA: enzyme-linked immunosorbent assay; HDL: high-density lipoprotein; hs-CRP: high-sensiti”
• Upregulation of ADAMTS-7 and downregulation of COMP are associated with aortic aneurysm (2017, unknown): “Wang et al (10) reported that ADAMTS‑7 facilitated vascular intimal hyperplasia via the degradation of COMP.”
• YIA3: ADAMTS7 CLEAVAGE AND VASCULAR SMOOTH MUSCLE CELL MIGRATION IS AFFECTED BY A CORONARY ARTERY DISEASE ASSOCIATED VARIANT (2013, background): “A recent study in rats demonstrated that ADAMTS7 facilitated vascular smooth muscle cell (VSMC) migration by degrading the extracellular matrix protein TSP5 and thereby promoted neointima formation following vascular mechanical injury.(6) Furthermore, in vitro studies have shown that VSMCs produce T”
• Biochemistry and physiological functions of ADAMTS7 metalloprotease (2013, background): “Unlike ADAM proteases, ADAMTS enzymes possess a central thrombospondin type 1-like repeat, which is thought to bind extracellular matrix (ECM) and sulfated glycosaminoglycans such as heparin and aggrecan 2, [37-40].”
• A disintegrin and metalloproteinase with thrombospondin motif 1 (ADAMTS1) expression increases in acute aortic dissection (2015, unknown): “…recently identified metalloproteinase family ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) has been implicated in the development and progression of many cardiovascular diseases (Jonsson-Rylander et al., 2005; Wagsater et al., 2008; Wang et al., 2009; Zhang et al., 2015).”
• Knockout of Adamts7, A Novel CAD Locus in Humans, Reduces Atherosclerosis in Mice (2015, background): “Adenoviral overexpression of ADAMTS7 increased COMP cleavage and neointima in injured arteries, whereas overexpression of COMP blocked ADAMTS7 effects.(13) Whether acute effects using transient overexpression extend to vascular pathophysiology and atherosclerosis during germline modulation has not b”