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

• Huajuan Shen ^[1] ; Qiang He ^[1] ; Yongze Dong ^[1] ; Lina Shao ^[1] ; Yueming Liu ^[1] ; Jianguang Gong ^[1]
  1. [1] Zhejiang Provincial People's Hospital

     Zhejiang Provincial People's Hospital

     China

     
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 35, Nº. 10, 2020, págs. 1125-1133
• Idioma: inglés
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• Resumen

  • 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.