Key result
Downregulated LINK-A lncRNA distinguishes diabetic nephropathy from healthy controls with an AUC of ~0.90.
Why the study?
LINK-A lncRNA is known to activate HIF1α in cancer, but its role and mechanism in diabetic nephropathy remain unclear.
Case-Control (n=84)
No
Effect estimate: AUC 0.9007 (95% CI 0.8109-0.9904)
LINK-A lncRNA may improve diabetic nephropathy by activating HIF1α signaling and inhibiting podocyte apoptosis.
Hypothesis-generating for biomarker use in diabetic nephropathy; animal data leave open human translation of HIF1α-targeted therapy.
Previous studies have revealed that long intergenic non-coding RNA for kinase activation (LINK-A), a long non-coding RNA (lncRNA) promotes disease progression in triple-negative breast cancer by activating hypoxia-inducible factor 1α (HIF1α). However, the activation of HIF1α has also been demonstrated to improve diabetic nephropathy. It is therefore reasonable to expect that LINK-A may also participate in diabetic nephropathy. In the current study, the expression of LINK-A lncRNA and HIF1α was determined in renal biopsies of patients with diabetic nephropathy. LINK-A lncRNA and HIF1α expression levels were detected by reverse transcription quantitative (RT-q) PCR and ELISA in diabetic patients without complications and used as controls. Correlations between LINK-A lncRNA and HIF1α expression were analyzed using Pearson's correlation coefficient. Effects of lncRNA and HIF1α overexpression on LINK-A lncRNA expression, HIF1α expression and cell apoptosis were assessed using RT-qPCR, western blotting and a cell apoptosis assay. The results revealed that LINK-A lncRNA and HIF1α were downregulated in patients with diabetic nephropathy, as well as in diabetic patients without complications. The lowest expression of LINK-A lncRNA and HIF1α were observed in healthy controls. A positive correlation was identified between LINK-A lncRNA and HIF1α in both patients groups, but not in the control group. LINK-A lncRNA and HIF1α overexpression inhibited the apoptosis of mouse podocyte cells under a high glucose treatment. LINK-A lncRNA overexpression also promoted HIF1α expression in mouse podocyte cells, while HIF1α overexpression did not significantly affect LINK-A lncRNA expression. In conclusion, LINK-A lncRNA may activate HIF1α signaling resulting in the improvement of diabetic nephropathy treatment.
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Yang et al. (2019) conducted a case-control in Diabetic nephropathy (n=84). LINK-A lncRNA expression vs. Healthy controls and diabetic patients without complications was evaluated on Diagnostic value of LINK-A lncRNA for diabetic nephropathy versus healthy controls (AUC 0.9007, 95% CI 0.8109-0.9904). LINK-A lncRNA was significantly downregulated in patients with diabetic nephropathy and distinguished them from healthy controls with an AUC of 0.9007.
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