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Article Open Access

MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner

  • Authors:
    • Xianggui Yang
    • Dongming Wu
    • Hongfei Du
    • Fang Nie
    • Xueli Pang
    • Ying Xu
  • View Affiliations / Copyright

    Affiliations: Department of Laboratory Medicine, The First Affiliated Hospital of Chengdu Medical University, Chengdu, Sichuan 610500, P.R. China
    Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1511-1519
    |
    Published online on: September 25, 2017
       https://doi.org/10.3892/ijmm.2017.3152
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Abstract

Transient receptor potential (TRP) cation channels are essential for normal cellular physiology, and their abnormal expression may lead to a number of disorders, including podocytopathy. Therefore, it is crucial to understand the mechanisms underlying the regulation of TRP channels. In the present study, microRNA (miR)-135a was found to be upregulated in patients with focal segmental glomerulosclerosis and mice treated with adriamycin (ADR). In cultured podocytes, transforming growth factor (TGF)-β and ADR were found to promote miR‑135a expression. Conversely, TRP channel 1 (TRPC1) protein levels were markedly downregulated in podocytes from mice treated with ADR, as well as in cultured podocytes treated with ADR and TGF-β. Ectopic expression of miR-135a led to severe podocyte injury and disarray of the podocyte cytoskeleton, whereas podocyte-specific expression of TRPC1 was able to reverse the pathological effects of miR-135a in cultured podocytes. Moreover, using luciferase reporter assays and western blot analysis, TRPC1 was identified as a target gene of miR-135a. To the best of our knowledge, this is the first study to demonstrate the role of TRPC1 in the development of podocyte injury and disorders of the podocyte cytoskeleton, which may contribute to the development of novel therapeutics for podocyte injury-associated kidney diseases.
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Copy and paste a formatted citation
Spandidos Publications style
Yang X, Wu D, Du H, Nie F, Pang X and Xu Y: MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner. Int J Mol Med 40: 1511-1519, 2017.
APA
Yang, X., Wu, D., Du, H., Nie, F., Pang, X., & Xu, Y. (2017). MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner. International Journal of Molecular Medicine, 40, 1511-1519. https://doi.org/10.3892/ijmm.2017.3152
MLA
Yang, X., Wu, D., Du, H., Nie, F., Pang, X., Xu, Y."MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner". International Journal of Molecular Medicine 40.5 (2017): 1511-1519.
Chicago
Yang, X., Wu, D., Du, H., Nie, F., Pang, X., Xu, Y."MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner". International Journal of Molecular Medicine 40, no. 5 (2017): 1511-1519. https://doi.org/10.3892/ijmm.2017.3152
Copy and paste a formatted citation
x
Spandidos Publications style
Yang X, Wu D, Du H, Nie F, Pang X and Xu Y: MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner. Int J Mol Med 40: 1511-1519, 2017.
APA
Yang, X., Wu, D., Du, H., Nie, F., Pang, X., & Xu, Y. (2017). MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner. International Journal of Molecular Medicine, 40, 1511-1519. https://doi.org/10.3892/ijmm.2017.3152
MLA
Yang, X., Wu, D., Du, H., Nie, F., Pang, X., Xu, Y."MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner". International Journal of Molecular Medicine 40.5 (2017): 1511-1519.
Chicago
Yang, X., Wu, D., Du, H., Nie, F., Pang, X., Xu, Y."MicroRNA-135a is involved in podocyte injury in a transient receptor potential channel 1-dependent manner". International Journal of Molecular Medicine 40, no. 5 (2017): 1511-1519. https://doi.org/10.3892/ijmm.2017.3152
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