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Published on: February 15, 2022
Hsa_circ_0007765 Promotes Platelet-Derived Growth Factor-BB-Induced Proliferation and Migration of Human Aortic
Shengwei Ma1, Haiyun Qian2, Qian Zhou1
1Surgical Department of Cardiothoracic Macrovascular, Jingzhou Hospital Affiliated to Yangtze University, No.26 Chuyuan Avenue, Jingzhou District, Jingzhou, 434020, Hubei, China.
Insights
This study reveals that circ_0007765 promotes atherosclerosis by enhancing human aortic vascular smooth muscle cell proliferation and migration. It achieves this by increasing Fibroblast Growth Factor Receptor Substrate 2 (FRS2) via sponging microRNA-654-3p.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Cell Biology
Background:
- Human aortic vascular smooth muscle cells (HA-VSMCs) are crucial in vascular disease pathogenesis, including atherosclerosis (AS).
- Circular RNAs (circRNAs) are increasingly recognized for their regulatory roles in HA-VSMC biological functions.
Purpose of the Study:
- To investigate the role and underlying mechanism of hsa_circRNA_102353 (circ_0007765) in platelet-derived growth factor-BB (PDGF-BB)-induced HA-VSMCs.
- To elucidate the interaction between circ_0007765, microRNA-654-3p (miR-654-3p), and Fibroblast Growth Factor Receptor Substrate 2 (FRS2) in this context.
Main Methods:
- Gene expression analysis using RT-qPCR for circ_0007765, miR-654-3p, and FRS2.
- Cellular function assays including MTT, EdU, Transwell, and wound healing to assess proliferation, invasion, and migration.
- Protein level assessment via Western blot and molecular interaction verification through dual-luciferase reporter and RNA pull-down assays.
Main Results:
- PDGF-BB stimulation significantly increased HA-VSMC proliferation, invasion, and migration.
- Circ_0007765 and FRS2 expression were upregulated, while miR-654-3p was downregulated in PDGF-BB-treated HA-VSMCs.
- Circ_0007765 knockdown inhibited PDGF-BB-induced HA-VSMC proliferation, invasion, and migration, with circ_0007765 acting as a sponge for miR-654-3p to upregulate FRS2.
Conclusions:
- Circ_0007765 promotes PDGF-BB-induced HA-VSMC proliferation and migration by upregulating FRS2 expression through sponging miR-654-3p.
- This circRNA-miRNA-mRNA axis presents a potential therapeutic target for atherosclerosis.
Abstract:
Human aortic vascular smooth muscle cells (HA-VSMCs) play vital roles in the pathogenesis of vascular diseases, including Atherosclerosis (AS). Circular RNAs (circRNAs) have been reported to regulate the biological functions of HA-VSMCs. Therefore, this study aimed to explore the role and mechanism of hsa_circRNA_102353 (circ_0007765) in platelet-derived growth factor-BB (PDGF-BB)-induced HA-VSMCs. Circ_0007765, microRNA-654-3p (miR-654-3p), and Fibroblast Growth Factor Receptor Substrate 2 (FRS2) expression were measured using real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferative ability, invasion, and migration were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), Transwell, and wound healing assays. CyclinD1, MMP2, and FRS2 protein levels were assessed using a Western blot assay. Binding between miR-654-3p and circ_0007765 or FRS2 was predicted by Circinteractome or TargetScan, and verified using dual-luciferase reporter and RNA pull-down assays. PDGF-BB induced HA-VSMC proliferation, invasion, and migration. Circ_0007765 and FRS2 expression levels were increased in PDGF-BB-treated HA-VSMCs, and the miR-654-3p level was reduced. Moreover, circ_0007765 absence hindered PDGF-BB-induced HA-VSMC proliferation, invasion, and migration in vitro. At the molecular level, circ_0007765 increased FRS2 expression by acting as a sponge for miR-654-3p. Our findings revealed that circ_0007765 boosted PDGF-BB-induced HA-VSMC proliferation and migration through elevating FRS2 expression via adsorbing miR-654-3p, providing a feasible therapeutic strategy for AS.
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