eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
Current issue Archive Manuscripts accepted About the journal Editorial board Abstracting and indexing Subscription Contact Instructions for authors Ethical standards and procedures
SCImago Journal & Country Rank
2/2021
vol. 46
 
Share:
Share:
more
 
 
abstract:
Experimental immunology

Knockdown of circular RNA hsa_circ_0003204 inhibits oxidative stress and apoptosis through the miR-330-5p/Nod2 axis to ameliorate endothelial cell injury induced by low-density lipoprotein

Bin Zhang
1
,
Yufan Zhang
1
,
Rui Li
1
,
Yan Li
1
,
Wei Yan
2

1.
Department of Neurology, Yulin First Hospital, Yulin, Shaanxi, China
2.
Department of Vasculocardiology, People’s Hospital of Tongchuan, Tongchuan, Shaanxi, China
Cent Eur J Immunol 2021; 46 (2): 140-151
Online publish date: 2021/08/07
View full text
Get citation
ENW
EndNote
BIB
JabRef, Mendeley
RIS
Papers, Reference Manager, RefWorks, Zotero
AMA
APA
Chicago
Harvard
MLA
Vancouver
 
Introduction
Atherosclerosis (AS) is the leading cause of cardiovascular disease. Circular RNA hsa_circ_0003204 (hsa_circ_0003204) was elevated in oxidized low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells. However, the role and molecular mechanism of hsa_circ_0003204 in the AS process have not been studied.

Material and methods
Human primary aortic endothelial cells (HAECs) were treated with low-density lipoprotein (ox-LDL) to establish the AS model. The viability of ox-LDL-induced HAECs was assessed by counting kit-8 (CCK8) assay. Reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) levels in ox-LDL-induced HAECs supernatant were evaluated with the relevant kits. The apoptosis of ox-LDL-induced HAECs was determined via flow cytometry assay. The expression of hsa_circ_0003204, miR-330-5p, and nucleotide-binding oligomerization domain 2 (Nod2) was analyzed through quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between hsa_circ_0003204 or Nod2 and miR-330-5p was verified by dual-luciferase reporter assay. Protein level of Nod2 was detected using western blot analysis.

Results
Hsa_circ_0003204 and Nod2 were upregulated while miR-330-5p was decreased in ox-LDL-induced HAECs. Hsa_circ_0003204 depletion restrained the oxidative stress and apoptosis of ox-LDL-induced HAECs. Notably, hsa_circ_0003204 regulated Nod2 expression via sponging miR-330-5p in HAECs. Moreover, miR-330-5p inhibition restored the constraint of the oxidative stress and apoptosis of ox-LDL-induced HAECs caused by hsa_circ_0003204 silencing. Additionally, miR-330-5p targeted Nod2 and Nod2 enhancement abolished the repressive effects of miR-330-5p overexpression on the oxidative stress and apoptosis of ox-LDL-induced HAECs.

Conclusions
Hsa_circ_0003204 exhaustion mitigated endothelial cell injury through suppressing the oxidative stress and apoptosis in ox-LDL-induced HAECs via the miR-330-5p/Nod2 axis.

keywords:

hsa_circ_0003204, miR-330-5p, Nod2, ox-LDL, AS

Quick links
© 2021 Termedia Sp. z o.o. All rights reserved.
Developed by Bentus.
PayU - płatności internetowe