Effects of LncRNA MYOSLID and MiR-29c-3p on the Proliferation and Migration of Angiotensin II-induced Vascular Smooth Muscle Cells

Atherosclerosis (ATH) represents a major cause of cardiovascular disease. Long noncoding RNA (LncRNA) myocardin-induced smooth muscle lncRNA, inducer of differentiation (MYOSLID) and microRNA (miR) -29c-3p show substantial roles in ATH. We investigated their regulatory mechanisms on vascular smooth muscle cell (VSMC) proliferation and migration.Angiotensin (Ang) II-induced VSMCs were used for in vitro research. The MYOSLID and miR-29c-3p expression patterns in VSMCs were assessed by reverse transcription-quantitative polymerase chain reaction. MYOSLID was overexpressed, or miR-29c-3p was silenced in VSMCs by cell transfection, followed by proliferation, migration, and apoptosis evaluation. The colocalization of MYOSLID and miR-29c-3p was observed by RNA in situ hybridization. The targeted binding relationship of miR-29c-3p and MYOSLID was verified by dual-luciferase and RNA immunoprecipitation assays. Joint experiments were performed with the overexpressed MYOSLID and miR-29c-3p via cotransfection. An ATH mouse model was established and injected with LV-MYOSLID, with the aortic root atherosclerotic lesion observed by HE staining and the α-SMA expression determined by immunohistochemistry.The MYOSLID expression was decreased, while the miR-29c-3p expression was increased in the Ang II-induced VSMCs, along with the promoted VSMC proliferation, apoptosis, and migration. Meanwhile, the MYOSLID overexpression or miR-29c-3p silencing repressed the Ang II-induced VSMC behaviors. The miR-29c-3p mimics reduced the luciferase activity of the MYOSLID 3'UTR-WT-transfected cells, but had no obvious influence on the MYOSLID 3'UTR-MUT-transfected cells. Overexpressed miR-29c-3p partially nullified the highly expressed MYOSLID-repressed Ang II-induced VSMC apoptosis, proliferation, and migration. The MYOSLID overexpression repressed the miR-29c-3p expression and reduced the atherosclerotic lesion area and the number of α-SMA-positive VSMCs in ATH mice.The MYOSLID overexpression restrained the Ang II-induced VSMC proliferation, migration, and apoptosis by repressing the miR-29c-3p expression, thus retarding the atherosclerotic plaque formation.