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Abstract
Purpose
The objective of this paper is to explore the role of circHECTD1 in vascular smooth muscle cells (VSMCs) and atherosclerosis (AS).
Methods
VSMCs were treated with platelet-derived growth factor-BB (PDGF-BB) in vitro, and the level of circHECTD1 was determined using qRT-PCR. Cell proliferation, migration, and invasion were analyzed using CCK8 and transwell assays. Cell apoptosis and cell cycle were analyzed using flow cytometry. The binding interaction between circHECTD1 and KHDRBS3 or EZH2 was investigated using the RIP, RNA pull-down.
Results
CircHECTD1 was upregulated in PDGF-BB-induced VSMCs with a dose-dependent and time-dependent manner. Knockdown of circHECTD1 suppressed VSMCsproliferation and migration and enhanced cell apoptosis in VSMCs, while circHECTD1 overexpression yielded opposite effects. Mechanistically, circHECTD1 could interact with KHDRBS3, thus enhanced the stability of EZH2 mRNA and increased EZH2 protein level. In addition, silencing EZH2 in VSMCs reversed the proliferation-enhancing effect of circHECTD1 overexpression.
Conclusion
Our findings provided providing a potential prognostic and therapy biomarker for AS.
Abbreviations
VSMCs, vascular smooth muscle cells; AS, atherosclerosis; PDGF-BB, platelet-derived growth factor-BB; circRNAs, Circular RNAs; HBVSMCs, human brain VSMCs; qRT-PCR, Quantitative reverse transcription-polymerase chain reaction; FISH, fluorescence in situ hybridization; RIP, RNA immunoprecipitation; RBPs, RNA binding proteins.
Data Sharing Statement
The datasets presented during the current study are available from the corresponding author on reasonable request.
Acknowledgments
The authors sincerely appreciate all lab members. Meina Feng and Wenxian Tu are co-first authors for this study.
Disclosure
The authors report no conflicts of interest in this work.