Effects of Long Noncoding RNA HOTAIR Targeting miR-138 on Inflammatory Response and Oxidative Stress in Rat Cardiomyocytes Induced by Hypoxia and Reoxygenation

• Published in: Disease markers 2021, Vol.2021, p.4273274-11
• Main Authors: Wang, Guofeng, Wang, Qi, Xu, Weixue
• Format: Article
• Language: English
• Subjects: Animals; Antisense RNA; Apoptosis; Cardiomyocytes; Cardiovascular disease; Cell culture; Cell Hypoxia - drug effects; Cell Hypoxia - genetics; Coronary vessels; Cytokines; Gene Expression Regulation; Heart; Hypoxia; Inflammation; Inflammation - genetics; Inflammatory response; Inhibitors; Ischemia; Medical research; MicroRNAs; MicroRNAs - genetics; Myocytes, Cardiac; NF-κB protein; Oxidative stress; Oxidative Stress - genetics; Oxygen - administration & dosage; Polymerase chain reaction; Proteins; Rats; Reporter gene; Ribonucleic acid; RNA; RNA, Long Noncoding - genetics; siRNA; Thrombosis; Tumor necrosis factor-TNF
• ISSN: 0278-0240; 1875-8630
• DOI: 10.1155/2021/4273274

Objective. To investigate the effects of HOX transcript antisense RNA (HOTAIR) and miR-138 on inflammatory response and oxidative stress (OS) induced by IRI in rat cardiomyocytes. Methods. H9C2 cells were divided into the control group, H/R group, H/R+siRNA NC group, H/R+si-HOTAIR group, and H/R+si-HOTAIR+inhibitor group. Expression levels of HOTAIR, miR-138, and inflammatory factors were detected by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The double luciferase reporter gene assay was used to detect the targeting relationship between HOTAIR and miR-138. Results. Compared with the control group, the level of miR-138 and SOD in the H/R group was obviously reduced, while the expression levels of the HOTAIR, MDA, and NF-κB pathway were obviously increased. Compared with the H/R group, the level of miR-138 and SOD in the H/R+si-HOTAIR group was obviously increased, and the expression levels of the HOTAIR, MDA, and NF-κB pathway were obviously decreased. Compared with the H/R+si-HOTAIR group, the level of SOD in the H/R+si-HOTAIR+inhibitor group decreased; MDA content and the NF-κB pathway expression level increased. In the double luciferase reporter gene assay, compared with the HOTAIR wt+NC group, the luciferase activity of the HOTAIR wt+miR-138 mimic group was obviously decreased. Conclusions. Silent HOTAIR can promote the expression of miR-138 and inhibit H/R-induced inflammatory response and OS by regulating the NF-κB pathway, thus protecting cardiomyocytes.