LncRNA XIST protects podocyte from high glucose-induced cell injury in diabetic nephropathy by sponging miR-30 and regulating AVEN expression

Abstract

Diabetic nephropathy (DN) is one of the most important complications of diabetes mellitus. Thus, it is urgent to develop a novel diagnosis or therapeutic strategy that could suspend DN progression. Moreover, there is increasing evidence demonstrating that long non-coding RNA (lncRNA) acts as critical players in regulating autophagy and are involved in DN. We demonstrated that lncRNA X-inactive specific transcript (XIST) was downregulated in high glucose (HG) treated podocytes, accompanied by increased apoptosis of podocytes. Overexpression of XIST significantly reduced the apoptosis and promoted the number of viable cells of podocyte under HG treatment. Prediction by Targets can and dual-luciferase reporter assay revealed the interaction between miR-30 and XIST and AVEN. Further WB (Western Blot), MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), and flow cytometry confirmed that XIST could reverse the expression of AVEN and ameliorate HG-induced apoptosis. In conclusion, our research revealed that XIST plays a protective effect on podocyte injury induced by HG through miR-30/AVEN axis.

Keywords:

• Diabetic nephropathy
• XIST
• MiR-30
• podocyte
• high glucose

Author contributions

LBD: Research idea and study design; LBD, WY, ZSQ, LLS: data acquisition; WY, ZSQ, LLS: data analysis/interpretation; WY, ZSQ, LLS: statistical analysis; LBD: supervision or mentorship.

Disclosure statement

No potential conflict of interest was reported by the author(s). Author initials take responsibility that this study has been reported honestly, accurately, and transparently, and accepts accountability for the overall work by ensuring that questions about the accuracy or integrity of any portion of the work are appropriately investigated and resolved.

Data availability statement

All data generated or analysed during this study are included in this article.

Additional information

Funding

The research was supported by National Science Foundation of China 81403172 and National Natural Science Foundation Grant 81860159.