LncRNA MALAT1 promotes the apoptosis and oxidative stress of human lens epithelial cells via p38MAPK pathway in diabetic cataract

Abstract

BackgroundLncRNAs are involved in various biological processes and disorders. We aimed to investigate the role of lncRNA MALAT1 deregulation in the pathogenic mechanism of diabetic cataract (DC). MethodsThe expression of MALAT1 in the tissues and cells was detected by qRT-PCR. The levels of SP1, p38 and apoptosis-related protein were assessed by Western blot assay. Chromatin immunoprecipitation assay and Dual luciferase assay were performed to evaluate the relationship between SP1 and MALAT1. The viability and apoptosis of human lens epithelial cells (HLECs) were analyzed by MTT assay and flow cytometry. The levels of malonyldialdehyde (MDA), superoxide dismutase (SOD) and phospholipid hydroperoxide glutathione peroxidase (GSH-Px) were used to examine the level of oxidative stress. ResultsMALAT1 not only was aberrantly expressed in DC anterior lens capsule tissues and high glucose (HG)-treated HLECs, but also were up-regulated by HG to promote the apoptosis and oxidative stress of HLECs. HG induced the up-regulation of MALAT1 via SP1 binding MALAT1 promoter regions in HLECs. Moreover, p38 was up-regulated in HG-treated HLECs, and knockdown of p38 reversed the effect of MALAT1 over-expression on HLECs. ConclusionHG induced the up-regulation of MALAT1 in HLECs via SP1 binding SP1 binding MALAT1, which promoted the apoptosis and oxidative stress of HLECs through the activation of p38MAPK signaling pathway.