LncRNA RNA ROR Aggravates Hypoxia/Reoxygenation-Induced Cardiomyocyte Ferroptosis by Targeting miR-769-5p/CBX7 Axis.

Abstract

Ferroptosis is a new way of cell death which is reported to participate in the pathology of myocardial ischemia-reperfusion (MI/R) injury, but it's mechanism remains unclear. The present investigation is to study the emerging role of long non-coding RNA (lncRNA) regulator of reprogramming (ROR) in cardiomyocyte ferroptosis after hypoxia/reoxygenation (H/R) administration. RT-qPCR and/or Western blot methods were performed to examine the gene/or protein levels, and CCK-8, ELISA, and DCFH-DA staining determined the cellular viability and ferroptosis. Dual-luciferase and RNA immunoprecipitation were applied to verify molecular interaction. LncRNA ROR and miR-769-5p were overexpressed and reduced in blood samples from MI patients and H/R-treated AC16 cells, respectively. Mechanistically, lncROR sponged to miR-769-5p, thus upregulating CBX7 expression. Functional experiments presented that lncRNA ROR silence mitigated H/R-stimulated inflammatory damage, oxidative stress, and ferroptosis in AC16 cells, whereas these roles could be reversed by co-downregulation of miR-769-5p or co-overexpression of CBX7. These data uncovered that lncRNA ROR prevented against H/R-induced cardiomyocyte ferroptosis by modulating miR-769-5p/CBX7 signaling, emphasizing the therapeutic value of lncRNA ROR in MI/R injury.

• Authors: Guorong Lai, Jie Shen, Yanhui Hu, Fan Yang, Chao Zhang, Dongsheng Le, Qin Liu, Yingping Liang
• Journal: Biochemical genetics (Biochem Genet) (Dec 29 2023) ISSN: 1573-4927 [Electronic] United States
• PMID: 38157079 (Publication Type: Journal Article)
• Copyright: © 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.