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

May 15, 2021Journal of cardiovascular pharmacology

Circ_CHFR helps blood vessel muscle cells grow and move in response to platelet growth factor through the miR-149-5p/NRP2 pathway

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Abstract

Circ_CHFR levels were elevated in PDGF-BB-induced human vascular smooth muscle cells (HVSMCs).

Silencing circ_CHFR reversed the promotion of cell proliferation, migration, and invasion caused by PDGF-BB in HVSMCs.
Circ_CHFR directly bound to microRNA (miR)-149-5p, which is associated with the effects of circ_CHFR knockdown.
Neuropilin 2 (NRP2) was identified as a target of miR-149-5p, suggesting a regulatory relationship.
Overexpression of miR-149-5p negated the PDGF-BB-induced enhancements of cell proliferation, migration, and invasion by targeting NRP2.
Circ_CHFR is linked to the miR-149-5p/NRP2 axis, implicating its role in the dysfunction of HVSMCs during atherosclerosis.

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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.

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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

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