Upregulation of miRNA-1228-3p alleviates TGF-β-induced fibrosis in renal tubular epithelial cells

Huajuan Shen, Qiang He, Yongze Dong, Lina Shao, Yueming Liu and Jianguang Gong

Department of Nephrology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, China

Offprint requests to: Huajuan Shen, Department of Nephrology, Zhejiang Provincial People's Hospital, 158 Shangtang Road, Hangzhou, Zhejiang 310014, China. e-mail: zryshenhuajuan@163.com

Summary. Background. Chronic kidney disease (CKD) has become a major public health issue, which can lead to renal fibrosis regardless of the initial injury. It has been previously reported that miRNA-1228-3p was correlate with the progression of kidney fibrosis. However, the mechanism by which miRNA-1228-3p regulates renal fibrosis remains unclear. Methods. Renal tubular epithelial cells (HK-2) were treated with TGF-β1 (10 ng/ml) in an in vitro model of renal fibrosis. Gene and protein expressions in HK-2 cells were measured by Western-blot and RT-qPCR, respectively. The relation between miRNA-1228-3p and its target gene was investigated by dual luciferase report analysis. Results. Upregulation of miRNA-1228-3p significantly inhibited TGF-β1-induced fibrosis of HK-2 cells in vitro by targeting GDF11. In addition, miRNA-1228-3p exhibited anti-fibrosis effect through inhibition of the smad2/smad4 signaling pathway. Conclusion. Upregulation of miRNA-1228-3p markedly inhibited the progression of renal fibrosis in vitro, indicating that miRNA-1228-3p may serve as a potential novel target for the treatment of renal fibrosis. Histol Histopathol 35, 1125-1133 (2020)

Key words: miRNA-1228-3p, Renal fibrosis, TGF-β1 signaling pathway

DOI: 10.14670/HH-18-242