ADAMTS-7 promotes vascular smooth muscle cells proliferation in vitro and in vivo
By Lu Zhang, F. Yu, Li Wang, Jingang Zheng, Yaoyao Du, Yaqian Huang, Bo Liu, Xian Wang, W. Kong. 2015
21 citations recorded by the source corpus.
Vascular smooth muscle cell (VSMC) proliferation and migration are pivotal for the pathogenesis of atherosclerosis and post-angioplasty restenosis. We have recently reported that a disintegrin and metalloproteinase with thrombospondin motifs-7 (ADAMTS-7), a novel metalloproteinase, contributes directly to neointima formation by mediating VSMC migration. However, whether ADAMTS-7 affects VSMC proliferation remains unclear. In this study, we found that luminal adenoviral delivery of ADAMTS-7 aggravated intimal hyperplasia 7 d after injury, paralleled by an increased percentage of PCNA-positive cells in both intima and media. In contrast, perivascular administration of ADAMTS-7 siRNA, but not scrambled siRNA to injured arteries attenuated intimal thickening at day 7, paralleled with reduced intimal VSMC replication, without alteration of VSMC proliferation in the media. In accordance, [3H]-thymidine incorporation assay in primary cultured rat VSMCs revealed an enhanced replication rate (by 61%) upon ADAMTS-7 overexpression and retarded proliferation (by 23%) upon ADAMTS-7 siRNA administration. Our data demonstrates that ADAMTS-7 promotes VSMC proliferation both in vitro and in vivo. ADAMTS-7 may therefore serve as a novel therapeutic target for atherosclerosis and post-angioplasty restenosis.
Subfields: Cancer Research, Immunology and Allergy, 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 promotes VSM proliferation both in vivo and in vitro [119].”
- 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).”