Up-regulation of miR-20a weakens inflammation and apoptosis in high-glucose-induced renal tubular cell mediating diabetic kidney disease by repressing CXCL8 expression

In our study, we determined the pattern of expression and biological roles of microRNA-20a (miR-20a) in diabetic kidney disease (DKD). The difference in the expression of miR-20a and proinflammatory genes (TNF-alpha, IL-6, and IL-1 beta) was measured across control, normal glucose (NG), and high glucose (HG) groups. Co-transfection miR-20a mimic and CXCL8 silence was used to assess the miR-20a/CXCL8 axis in the HG-induced HK-2 cell injury involved in DKD. miR-20a in HG group was significantly decreased, and a marked augmentation of inflammatory factor gene expression (TNF-alpha, IL-6, and IL-1 beta) in HK-2 cells was induced by HG. miR-20a over-expression enhanced cell proliferation, inhibited cell apoptosis, and suppressed the inflammatory response of HK-2 cells. CXCL8 knockdown strengthened the role of miR-20a. Our findings showed that miR-20a might be a significant regulator of HG-induced renal proximal tubular inflammatory injury mediating diabetic kidney disease through regulation of the expression of CXCL8 and the MEK/ERK pathway.

Automated summary

This study determined the expression pattern and biological roles of miR-20a in diabetic kidney disease (DKD). miR-20a over-expression enhanced cell proliferation, inhibited cell apoptosis, and suppressed the inflammatory response. Additionally, miR-20a may regulate HG-induced renal proximal tubular inflammatory injury through the regulation of CXCL8 expression and the MEK/ERK pathway.