LNCRNA OIP5-AS1 regulates oxidative low-density lipoprotein-mediated endothelial cell injury via miR-320a/LOX1 axis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2020-02-18

AUTHORS

Chunmei Zhang, Hailing Yang, Yan Li, Pengfei Huo, Piyong Ma

ABSTRACT

An increasing amount of research showed that endothelial cells (ECs) play crucial role in vascular disorders such as atherosclerosis (AS). LncRNA OIP5-AS1 and microRNA-320a (miR-320a) were reported to exert function in ECs. The purpose of this research was to investigate the functional mechanism of OIP5-AS1 and miR-320a in ox-LDL-treated HUVECs. The RNA levels of OIP5-AS1, miR-320a, and Lectin-like oxidized low-density lipoprotein receptor 1 (LOX1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of LOX1 and cell apoptosis-related genes were determined by Western blot assay. In addition, Cell Counting Kit-8 (CCK-8) and flow cytometry analysis were used to assess cell viability and apoptosis, respectively. Lactate dehydrogenase (LDH) activity was measured using LDH release assay. Besides, the interaction between miR-320a and OIP5-AS1 or LOX1 was predicted by starbase and verified by the dual-luciferase reporter assay. OIP5-AS1 expression was increased and miR-320a expression was decreased in oxidative low-density lipoprotein (ox-LDL)-treated HUVECs. OIP5-AS1 knockdown upregulated ox-LDL-treated HUVECs viability and suppressed apoptosis as well as LDH release. Interestingly, OIP5-AS1 elevated LOX1 level through downregulating miR-320a expression. As expected, miR-320a modulated LOX1 expression to mediate ox-LDL-treated HUVECs progression. Furthermore, OIP5-AS1 knockdown modulated cell progression via regulating miR-320a/LOX1 axis in ox-LDL-treated HUVECs. Our results demonstrated that the depletion of OIP5-AS1 enhanced cell viability and repressed apoptosis as well as LDH release in ox-LDL-treated HUVECs, providing potential target for the treatment of AS. More... »

PAGES

15-25

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11010-020-03688-9

DOI

http://dx.doi.org/10.1007/s11010-020-03688-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1124958022

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/32072428


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