Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages

Abstract

Long non-coding RNA OIP5-AS1 (lncRNA OIP5-AS1) and microRNA-128-3p (miRNA-128-3p) have been reported to play significant roles in human diseases. However, their role in atherosclerosis (AS) has been less studied. The aim of this research was to reveal the roles and functional mechanisms of OIP5-AS1 and miRNA-128-3p in AS development. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assays were performed to detect gene expression. Cell proliferation and apoptosis were assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. In addition, ELISA was employed to determine the levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. Oxidative stress was examined using a relevant kit. Furthermore, the interaction between miR-128-3p and OIP5-AS1 or cyclin-dependent kinase inhibitor 2A (CDKN2A) was predicted using StarBase, and then confirmed using the dual-luciferase reporter assay or the RNA immunoprecipitation (RIP) assay. We found that OIP5-AS1 and CDKN2A levels were upregulated and the miR-128-3p level was downregulated in oxidized low-density lipoprotein (ox-LDL)-induced THP1 cells. OIP5-AS1 knockdown weakened the regulatory effect of ox-LDL on cell progression. Interestingly, OIP5-AS1 directly interacted with miR-128-3p and miR-128-3p-targeted CDKN2A. Furthermore, OIP5-AS1 regulated ox-LDL-induced cell progression through modulating miR-128-3p expression, and miR-128-3p exerted its influence by modulating the CDKN2A level. Finally, we confirmed that OIP5-AS1 suppressed miR-128-3p expression to increase the level of CDKN2A. In conclusion, our findings demonstrate that OIP5-AS1 knockdown repressed the effect of ox-LDL on cell progression through regulating the miR-128-3p/CDKN2A axis, providing a potential target for the treatment of AS.