Open AccessRole of microRNA-29b in angiotensin II-induced epithelial-mesenchymal transition in renal tubular epithelial cells
Author(s) -
Jialin Pan,
Juhong Zhang,
Xingwei Zhang,
Xi Zhou,
Shengyue Lu,
Xiaoyan Huang,
Jun Shao,
Guo-qiang Lou,
Deye Yang,
YongJian Geng
Publication year - 2014
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2014.1935
Subject(s) - downregulation and upregulation , epithelial–mesenchymal transition , angiotensin ii , transfection , oncogene , endocrinology , medicine , transforming growth factor , microrna , apoptosis , chemistry , cancer research , biology , receptor , cell cycle , cell culture , gene , biochemistry , genetics
Angiotensin II (Ang II) has been proven to induce epithelial-mesenchymal transition (EMT). The aim of the present study was to determine the role of microRNA-29b (miR-29b) during Ang II-induced EMT. For this purpose, we used spontaneously hypertensive rats (SHRs) and age-matched Wistar-Kyoto (WKY) rats. The levels of Ang II and its receptor in the kidneys of the SHRs are significantly higher than those in the age-matched WKY rats. As shown by RT-qPCR, the expression of miR-29b in the renal cortex was lower in the SHRs than in the WKY rats. For in vitro experiments, NRK-52E renal tubular epithelial cells were treated with 10(-7) M Ang II; we found that the expression of miR-29b was decreased in the cells treated with Ang II. In addition, transfection of the NRK-52E cells with miR-29b inhibitor led to the downregulation of miR-29b in these cells, and increased the expression of transforming growth factor (TGF)-β, α-smooth muscle actin (α-SMA) and collagen I (Col I). Similar results were observed with the induction of Ang II expression in the NRK-52E cells. By contrast, the upregulation of miR-29b by transfection with miR-29b mimics inhibited the overexpression of these genes induced by Ang II. These results suggest that miR-29b plays an important role in Ang II-induced EMT.