mir-411 suppressed vein wall fibrosis by downregulating mmp-2 via targeting hif-1α

This study was aim to investigate the specific mechanisms of mir-411 in vein wall fibrosis remodeling. vein wall fibrosis injury-induced deep venous thrombosis (dvt) rat model was well established. the expression of mir-411 at mrna levels and collagen i, hypoxia-inducible factor (hif)-1α together with matrix metalloproteinase (mmp)-2 at protein levels in vein wall tissues and vascular smooth muscle cells (vsmcs) following transfection were determined using quantitative real-time pcr (qrt-pcr) and western blotting, respectively. luciferase reporter assay was used to confirm the potential target of mir-411. mir-411 mimic injected into rat model of dvt was to verify the role of mir-411 in vein wall fibrosis in vivo. mir-411 was downregulated while collagen i, hif-1α and mmp-2 was upregulated in vein wall tissues and vsmcs obtained from rat model of dvt. mir-411 overexpression in vsmcs separated from rats of vascular remodeling group (vr-vsmcs) upregulated mir-411, hif-1α and inhibited cell proliferation and collagen i expression, while mir-411 knockdown in vsmcs isolated from healthy rats (control-vsmcs) reversed the effects. furthermore, luciferase reporter assay demonstrated that hif-1α was a target of mir-411. in addition, overexpression of mir-411 and hif-1α in vr-vsmcs promoted hif-1α, collagen i expression and cell proliferation, however, tissue inhibitor of metalloproteinase (timp)-2 treatment led to adverse trends. mir-411 mimic injected into rat model of dvt could suppress vein wall fibrosis in vivo. mir-411 inhibited vein wall fibrosis by downregulating mmp-2 mediated by hif-1α.