Extracellular vesicle-mediated transfer of lncRNA CLDN10-AS1 aggravates low-density lipoprotein-induced vascular endothelial injury-Reference-Cited by-同舟云学术

Extracellular vesicle-mediated transfer of lncRNA CLDN10-AS1 aggravates low-density lipoprotein-induced vascular endothelial injury

Published:2022-12-01 Issue:12 Volume:54 Page:471-485
ISSN:1094-8341
Container-title:Physiological Genomics
language:en
Short-container-title:Physiological Genomics

Author:

Fu Xiaoyang¹²³⁴,Liu Heng¹,Fan Yulong¹,Yuan Ji³⁴⁵⁶^ORCID

Affiliation:

1. Department of Vascular Surgery, Henan Provincial People’s Hospital, Zhengzhou, China

2. People’s Hospital of Zhengzhou University, Zhengzhou, China

3. Central China Fuwai Hospital of Zhengzhou University, Zhengzhou, China

4. School of Clinical Medicine, Henan University, Zhengzhou, China

5. Department of Anaesthesia, Henan Provincial People’s Hospital, Zhengzhou, China

6. Department of Anaesthesia, Central China Fuwai Hospital, Zhengzhou, China

Abstract

Oxidized low-density lipoprotein (ox-LDL) stimulation impairs the oxidation-reduction equilibrium in vascular endothelial cells (VECs) and contributes to atherosclerosis (AS). This study probed the mechanisms of extracellular vesicle (EV)-mediated transfer of lncRNA CLDN10 antisense RNA 1 (CLDN10-AS1) in ox-LDL-induced VEC injury. Initially, VEC injury models were established by treating human umbilical vein endothelial cells (HUVECs) with ox-LDL. EVs were isolated from HUVECs (HUVECs-EVs) and identified. CLDN10-AS1, microRNA (miR)-186, and Yin Yang 1 (YY1) expressions in ox-LDL-treated HUVECs and EVs derived from these cells (ox-EVs) were measured. HUVECs were incubated with EVs, after which the cell viability, apoptosis, and concentrations of proinflammatory cytokines and oxidative stress markers were measured. We discovered that CLDN10-AS1 and YY1 were upregulated in ox-LDL-treated HUVECs, whereas miR-186 was downregulated. ox-EVs treatment elevated CLDN10-AS1 expression in HUVECs and ox-EVs overexpressing CLDN10-AS1 promoted VEC injury. Besides, CLDN10-AS1 is competitively bound to miR-186 and promoted YY1 expression. Rescue experiments revealed that miR-186 overexpression or YY1 suppression partially reversed the roles of ox-EVs overexpressing CLDN10-AS1 in ox-LDL-induced VEC injury. Lastly, clinical serum samples were collected for verification. Overall, CLDN10-AS1 carried by HUVECs-EVs into HUVECs competitively bound to miR-186 to elevate YY1 expression, thereby aggravating ox-LDL-induced VEC injury.

Funder

Henan Medical Science and Technology

Publisher

American Physiological Society

Subject

Genetics,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/physiolgenomics.00094.2022

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