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Αλέξανδρος Γ. Σφακιανάκης

Thursday, June 10, 2021

MicroRNA-125b inhibits the proliferation of vascular smooth muscle cells induced by platelet-derived growth factor BB

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Exp Ther Med. 2021 Aug;22(2):791. doi: 10.3892/etm.2021.10223. Epub 2021 May 24.

ABSTRACT

Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) is the main cause of arteriosclerosis obliterans (ASO). The present study aimed to investigate the role of microRNA (miR)-125b on the proliferation and migration of VSMCs. Platelet-derived growth factor-BB (PDGF-BB; 20 ng/ml) was used to treat VSMCs to establish an in vitro model of ASO. VSMCs were transfected with miR-125b mimic to overexpress miR-125. Cell Counting kit-8 (CCK-8) and BrdU assays were performed to assess the proliferative ability of VSMCs, while Transwell and wound healing assays were performed to assess the migratory ability of VSMCs. Western blot and immunofluorescence analyses were performed to detect the expression levels of angio-associated migratory cell protein (AAMP) and serum response factor (SRF) in VSMCs following transfection with miR- 125b mimic or inhibitor. The results demonstrated that miR-125b expression decreased following treatment with PDGF-BB, the effects of which were reversed following transfection with miR-125b mimic. According to the CCK-8 assay, the cell proliferative ability decreased by ~50% compared with the negative control (NC) group, and ~40% at day 4 based on the BrdU assay. The results of the Transwell and wound healing assays indicated that the migratory ability of VSMCs significantly decreased in the miR-125b mimic group compared with the NC group. Furthermore, western blot and immunofluorescence analyses demonstrated that AAMP and SRF expression levels decreased following transfection with miR-125b mimic compared with the NC group, the effects of which were reversed following transfection with miR-125 inhibitor. Taken together, the results of the present study suggested that miR-125b inhibits the proliferative and migratory abilities of VSMCs by regulating the expression levels of AAMP and SRF.

PMID:34093747 | PMC:PMC8170660 | DOI:10.3892/etm.2021.10223

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