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MiR-513a-5p Aggravates Atherosclerosis Phenotype by Downregulating TFPI2 in Vitro

Chun Wang, View ORCID ProfileFeng Yao
doi: https://doi.org/10.1101/2021.11.30.470524
Chun Wang
1Outpatient Office, The Sixth Hospital of Wuhan, Affiliated Hospital of Jianghan University, Wuhan 430015, Hubei, China
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Feng Yao
2Fourth Department of Integrated Diagnostics & Therapeutics, The Sixth Hospital of Wuhan, Affiliated Hospital of Jianghan University, Wuhan 430015, Hubei, China
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  • For correspondence: fengyao3228@163.com
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Abstract

Background Atherosclerosis (AS) induced cardiology disease is largely associated with morbidity and mortality. The dysfunction of vascular smooth muscle cells (VSMCs) is considered to contribute to the etiology of AS. However, the mechanism underlying VSMCs dysfunction remains largely unclear. Our study aimed to explore novel molecules mediating VSMCs function.

Methods Bioinformatical analysis was applied to identify the key miRNAs that was aberrantly expressed in AS mouse and potentially targeted TFPI2. The AS-like cell model was generated by treating VSMCs with ox-LDL. The expression level of miR-513a-5p and TFPI2 in VSMCs and the serum of AS patients was evaluated by RT-qPCR, and the expression level of TFPI2 and PCNA was measured by western blot. The cell viability and migration capacity of VSMCs were determined by CCK-8 and wound healing assay, respectively. The target relationship between miR-513a-5p and TFPI2 was validated by dual-luciferase assay.

Results MiR-513a-5p was highly expressed while TFPI2 presented a low expression in AS patient serum. Treatment with 100 μg/mL ox-LDL overtly facilitated the cell viability and migration of VSMCs, also promoted miR-513a-5p expression while limit the expression of TFPI2. Moreover, silencing miR-513a-5p inhibited the cell viability, migration and the expression of proliferative marker in ox-LDL treated VSMCs, while inhibition of TFPI2 enhanced that. It was further found that miR-513a-5p could target TFPI2 and silencing miR-513a-5p compromised the aggresive effect of TFPI2 inhibition on the viability and migration ox-LDL treated VSMCs.

Conclusion miR-513a-5p could contribute to the dysfunction of VSMCs in AS through targeting and inhibiting TFPI2.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted November 30, 2021.
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MiR-513a-5p Aggravates Atherosclerosis Phenotype by Downregulating TFPI2 in Vitro
Chun Wang, Feng Yao
bioRxiv 2021.11.30.470524; doi: https://doi.org/10.1101/2021.11.30.470524
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MiR-513a-5p Aggravates Atherosclerosis Phenotype by Downregulating TFPI2 in Vitro
Chun Wang, Feng Yao
bioRxiv 2021.11.30.470524; doi: https://doi.org/10.1101/2021.11.30.470524

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