LINC00462 is involved in high glucose‐induced apoptosis of renal tubular epithelial cells via AKT pathway.

New evidences suggest that long non‐coding RNAs (lncRNAs) may play important roles in a variety of kidney diseases, including diabetic nephropathy (DN). Our present study investigated the potential function of LINC00462 in high glucose (HG)‐induced apoptosis of renal tubular epithelial cells (RTEC) and to determine the underlying mechanism. The expression of LINC00462 in renal biopsy tissues was examined using quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR). Then, a loss of function assay was performed to determine the protective effect of LINC00462 in HG‐induced RTEC damage. In addition, the downstream signaling pathway of LINC00462 was also investigated. The qRT‐PCR results showed that the expression of LINC00462 was significantly up‐regulated in renal biopsies from DN patients. At the same time, LINC00462 was enhanced in a glucose concentration‐ and time‐dependent manner in human kidney (HK‐2 and HKC) cells subjected to HG treatment. The knockdown of LINC00462 improved the significantly reduced cell viability of HG treatment, decreased HG‐induced reactive oxygen species (ROS) and malondialdehyde levels, and up‐regulated the response of antioxidant systems to ROS by increasing superoxide dismutase and catalase levels. In addition, knockdown of LINC00462 inhibited HG‐induced cell apoptosis and affected the expression of apoptosis‐related proteins. Most importantly, we found that knockdown of LINC00462 enhanced the expression of p‐AKT. Moreover, AKT‐specific inhibitor LY294002 restored the effect of LINC00462 knockdown on apoptosis. In conclusion, our study demonstrated that knockdown of LINC00462 can ameliorate oxidative stress and apoptosis in HG‐induced RTEC by activating the AKT pathway, suggesting that knockdown of LINC00462 may provide a potential therapeutic approach for DN. [ABSTRACT FROM AUTHOR]