Key result
Knockdown of LINC00462 ameliorated oxidative stress and apoptosis in high glucose-induced renal tubular epithelial cells by activating the AKT pathway.
Why the study?
Long non-coding RNAs may play important roles in diabetic nephropathy, but the potential function and underlying mechanism of LINC00462 in high glucose-induced renal tubular epithelial cell apoptosis were unclear.
Does knockdown of LINC00462 reduce high glucose-induced apoptosis and oxidative stress in renal tubular epithelial cells?
Does knockdown of LINC00462 reduce high glucose-induced apoptosis and oxidative stress in renal tubular epithelial cells?
Knockdown of LINC00462 ameliorates oxidative stress and apoptosis in high glucose-induced renal tubular epithelial cells by activating the AKT pathway, suggesting a potential therapeutic target for diabetic nephropathy.
Potential target in diabetic nephropathy models; hypothesis-generating and requires in vivo and clinical validation.
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.
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Wang et al. (2019) studied Diabetic nephropathy. Knockdown of LINC00462 vs. High glucose treatment without knockdown was evaluated on Cell viability, oxidative stress, and apoptosis. Knockdown of LINC00462 ameliorated oxidative stress and apoptosis in high glucose-induced renal tubular epithelial cells by activating the AKT pathway.
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