miR-29b regulates Ang II-induced EMT of rat renal tubular epithelial cells via targeting PI3K/AKT signaling pathway

  • Authors:
    • Hongtao Hu
    • Shuang Hu
    • Shen Xu
    • Yue Gao
    • Fang Zeng
    • Hua Shui
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  • Published online on: March 22, 2018     https://doi.org/10.3892/ijmm.2018.3579
  • Pages: 453-460
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Abstract

Renal interstitial fibrosis is a necessary step in the progression of chronic kidney to end stage renal disease. MicroRNA-29 (miR-29) has been shown to play essential roles in epithelial-mesenchymal transition (EMT), and thus may contribute to the regulation of renal interstitial fibrosis. However, the role of miR-29 in the regulation of EMT during chronic kidney disease and renal transplantation has been a source of intense debate, and the mechanisms underlying this process are incompletely understood. In this study, we investigated the function of miR-29b in the regulation of EMT and to gain a better understanding of the mechanism by which miR-29b modulates EMT by targeting the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway during the process of renal interstitial fibrosis. The rat proximal tubular epithelial cell line NRK-52E was cultured in DMEM and treated with angiotensin II (Ang II) at various concentrations. RT-PCR was performed to investigate changes in the levels of expression of miR-29b in NRK-52E cells and western blotting was used to analyze the expression of PI3K, p-AKT, vimentin and keratin 18. The result of the study show that treatment of NRK-52E cells with Ang II induced the transition of the cellular phenotype from epithelial to mesenchymal and upregulated the PI3K/AKT signaling pathway; this was also found following treatment with a phosphatase and tensin homolog on chromosome 10 (PTEN)-specific inhibitor. Increased expression of miR-29b was able to reverse the phenotype induced by Ang II in NRK-52E cells and blocking miR-29b activity with an miR-29b inhibitor resulted in enhanced EMT. Additionally, the PI3K/AKT signaling pathway was found to be suppressed in the presence of enhanced expression of miR-29b by direct binding to 3'-untranslated region (3'-UTR) of PIK3R2. We concluded that miR-29b plays an important role in the negative regulation of Ang II-induced EMT via PI3K/AKT signaling pathway and propose that enhancing miR-29b level or blocking PI3K/AKT signaling pathway may be a novel therapeutic target in renal interstitial fibrosis.
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July-2018
Volume 42 Issue 1

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Hu H, Hu S, Xu S, Gao Y, Zeng F and Shui H: miR-29b regulates Ang II-induced EMT of rat renal tubular epithelial cells via targeting PI3K/AKT signaling pathway. Int J Mol Med 42: 453-460, 2018
APA
Hu, H., Hu, S., Xu, S., Gao, Y., Zeng, F., & Shui, H. (2018). miR-29b regulates Ang II-induced EMT of rat renal tubular epithelial cells via targeting PI3K/AKT signaling pathway. International Journal of Molecular Medicine, 42, 453-460. https://doi.org/10.3892/ijmm.2018.3579
MLA
Hu, H., Hu, S., Xu, S., Gao, Y., Zeng, F., Shui, H."miR-29b regulates Ang II-induced EMT of rat renal tubular epithelial cells via targeting PI3K/AKT signaling pathway". International Journal of Molecular Medicine 42.1 (2018): 453-460.
Chicago
Hu, H., Hu, S., Xu, S., Gao, Y., Zeng, F., Shui, H."miR-29b regulates Ang II-induced EMT of rat renal tubular epithelial cells via targeting PI3K/AKT signaling pathway". International Journal of Molecular Medicine 42, no. 1 (2018): 453-460. https://doi.org/10.3892/ijmm.2018.3579