Abstract

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-α, IL-6, and IL-1β) 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-α, IL-6, and IL-1β) 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.

摘要

在我们的研究中，我们确定了 microRNA-20a (miR-20a) 在糖尿病肾病 (DKD) 中的表达模式和生物学作用。在对照组、正常葡萄糖 (NG) 和高葡萄糖 (HG) 组中测量 miR-20a 和促炎基因（TNF-α、IL-6 和 IL-1β）的表达差异。共转染 miR-20a 模拟物和 CXCL8 沉默用于评估 HG 诱导的与 DKD 相关的 HK-2 细胞损伤中的 miR-20a/CXCL8 轴。HG 组 miR-20a 显着降低，HG 诱导 HK-2 细胞中炎症因子基因表达（TNF-α、IL-6 和 IL-1β）显着增加。miR-20a过表达增强细胞增殖，抑制细胞凋亡，并抑制HK-2细胞的炎症反应。CXCL8 敲低加强了 miR-20a 的作用。