Role of microRNA-29b in angiotensin II-induced epithelial-mesenchymal transition in renal tubular epithelial cells | Zendy

Jialin Pan | Zendy; Juhong Zhang | Zendy; Xingwei Zhang | Zendy; Xi Zhou | Zendy; Shengyue Lu | Zendy; Xiaoyan Huang | Zendy; JiaYu Shao | Zendy; Guoqiang Lou | Zendy; Deye Yang | Zendy; YongJian Geng | Zendy

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Role 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,

JiaYu Shao,

Guoqiang 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.

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