COL6A1 knockdown suppresses cell proliferation and migration in human aortic vascular smooth muscle cells

Vascular smooth muscle cell (VSMC) migration is an important pathophysiological signature of neointimal hyperplasia. The aim of the present study was to investigate the effects of collagen type VI α1 chain (COL6A1) on VSMC migration. COL6A1 expression was silenced in platelet-derived growth factor (PDGF-BB)-stimulated VSMCs. Cell counting kit-8, wound healing and Transwell assays were used to measure cell viability, migration and invasion, respectively. Reverse transcription-quantitative PCR and western blot analysis were performed to analyze the expression of factors associated with metastasis. COL6A1 silencing attenuated PDGF-BB-induced increases in cell viability and invasive abilities of VSMCs, in addition to partially reversing the increased expression of fibronectin (FN), matrix metalloproteinase (MMP)-2 and MMP-9 induced by PDGF-BB stimulation. The silencing of COL6A also overturned PDGF-BB-induced reduction in tissue inhibitor of metalloproteinase 2 expression in VSMCs. PDGF-BB activated the AKT/mTOR pathway, which was also inhibited by COL6A1 knockdown. Taken together, these findings suggest that COL6A1 silencing inhibited VSMC viability and migration by inhibiting AKT/mTOR activation.