The inhibition of calpains ameliorates vascular restenosis through MMP2/TGF-β1 pathway.
Ontology highlight
ABSTRACT: Restenosis limits the efficacy of vascular percutaneous intervention, in which vascular smooth muscle cell (VSMC) proliferation and activation of inflammation are two primary causal factors. Calpains influence VSMC proliferation and collagen synthesis. However, the roles of calpastatin and calpains in vascular restenosis remain unclear. Here, restenosis was induced by ligating the left carotid artery, and VSMCs were pretreated with platelet-derived growth factor (PDGF)-BB. Adenovirus vector carrying MMP2 sequence and specific small interfering RNA against calpain-1/2 were introduced. Finally, restenosis enhanced the expression of calpain-1/2, but reduced calpastatin content. In calpastatin transgenic mice, lumen narrowing was attenuated gradually and peaked on days 14-21. Cell proliferatio
SUBMITTER: Tang L
PROVIDER: S-EPMC4958998 | biostudies-literature | 2016 Jul
REPOSITORIES: biostudies-literature
ACCESS DATA