Circ_CHFR Promotes Platelet-Derived Growth Factor-BB–Induced Proliferation, Invasion, and Migration in Vascular Smooth Muscle Cells via the miR-149-5p/NRP2 Axis. Issue 1 (January 2022)

• Record Type: Journal Article
• Authors: Wang, Meixue; Li, Chengliang; Cai, Tianzhi; Zhang, Anji; Cao, Jinlong; Xin, Hong
• Is Part Of: Journal of cardiovascular pharmacology. Volume 79:Issue 1(2022)
• Publication Date: 2022-01
• Subjects: circ_CHFR -- HVSMC -- miR-149-5p -- NRP2 -- atherosclerosis -- proliferation; Cardiovascular Diseases -- drug therapy -- Periodicals; Cardiovascular System -- drug effects -- Periodicals; Cardiovascular pharmacology -- Periodicals; Cardiovascular agents -- Periodicals; Cardiovascular agents; Cardiovascular pharmacology; Periodicals; 615.7105
• DOI: 10.1097/FJC.0000000000001055
• Languages: English
• ISSNs: 0160-2446

Abstract

Abstract : Abstract: Circular RNA checkpoint with forkhead and ring finger domains (circ_CHFR) were reported to regulate vascular smooth muscle cell (VSMC) dysfunction during atherosclerosis (AS). However, the molecule mechanism of circ_CHFR in AS remains largely unclear. Human VSMCs (HVSMCs) were exposed to platelet-derived growth factor-BB (PDGF-BB) in vitro. Levels of circ_CHFR, microRNA (miR)-149-5p, and neuropilin 2 (NRP2) were determined using quantitative real-time polymerase chain reaction and western blot. Cell proliferation, migration, and invasion were analyzed using cell counting kit-8, colony formation, flow cytometry, wound healing, and transwell assays. The binding interaction between miR-149-5p and circ_CHFR or NRP2 was investigated using the dual-luciferase reporter and RNA immunoprecipitation assays. Circ_CHFR was elevated in PDGF-BB–induced HVSMCs in a dose-independent manner. Silencing of circ_CHFR reversed PDGF-BB–evoked promotion of cell proliferation, migration and invasion, as well as suppression of cell apoptosis in HVSMCs. Mechanistically, circ_CHFR directly bound to miR-149-5p, and miR-149-5p inhibition attenuated the effects of circ_CHFR knockdown on PDGF-BB–induced HVSMCs. Besides, NRP2 was confirmed to be a target of miR-149-5p, and circ_CHFR could regulate NRP2 expression through sponging miR-149-5p. Moreover, miR-149-5p overexpression abolished PDGF-BB–triggered enhancement of cell proliferation, migration, and invasion by targeting NRP2. Circ_CHFR promoted the proliferation, invasion, and migration of PDGF-BB–induced HVSMCs through miR-149-5p/NRP2 axis, providing a new insight into the pathogenesis of AS and a potential therapeutic target for AS treatment.