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miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling

  • Authors:
    • Chuan Qu
    • Xin Liu
    • Tianxin Ye
    • Linglin Wang
    • Steven Liu
    • Xingyu Zhou
    • Gang Wu
    • Jian Lin
    • Shaobo Shi
    • Bo Yang
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China
    Copyright: © Qu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5345-5352
    |
    Published online on: April 30, 2019
       https://doi.org/10.3892/mmr.2019.10200
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Abstract

Myofibroblast transdifferentiation is an important feature of cardiac fibrosis. Previous studies have indicated that microRNA‑216a (miR‑216a) is upregulated in response to transforming growth factor‑β (TGF‑β) in kidney cells and can activate Smad3; however, its role in myofibroblast transdifferentiation remains unclear. The present study aimed to investigate the role of miR‑216a in TGF‑β‑induced myofibroblast transdifferentiation, and to determine the underlying mechanisms. Adult mouse cardiac fibroblasts were treated with TGF‑β to induce myofibroblast transdifferentiation. An antagomir and agomir of miR‑216a were used to inhibit or overexpress miR‑216a in cardiac fibroblasts, respectively. Myofibroblast transdifferentiation was evaluated based on the levels of fibrotic markers and α‑smooth muscle actin expression. The miR‑216a antagomir attenuated, whereas the miR‑216a agomir promoted TGF‑β‑induced myofibroblast transdifferentiation. Mechanistically, miR‑216a accelerated myofibroblast transdifferentiation via the AKT/glycogen synthase kinase 3β signaling pathway, independent of the canonical Smad3 pathway. In addition, it was observed that miR‑216a activated AKT via the downregulation of PTEN. In conclusion, miR‑216a was involved in the regulation of TGF‑β‑induced myofibroblast transdifferentiation, suggesting that targeting miR‑216a may aid in developing effective interventions for the treatment of cardiac fibrosis.
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Copy and paste a formatted citation
Spandidos Publications style
Qu C, Liu X, Ye T, Wang L, Liu S, Zhou X, Wu G, Lin J, Shi S, Yang B, Yang B, et al: miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling. Mol Med Rep 19: 5345-5352, 2019.
APA
Qu, C., Liu, X., Ye, T., Wang, L., Liu, S., Zhou, X. ... Yang, B. (2019). miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling. Molecular Medicine Reports, 19, 5345-5352. https://doi.org/10.3892/mmr.2019.10200
MLA
Qu, C., Liu, X., Ye, T., Wang, L., Liu, S., Zhou, X., Wu, G., Lin, J., Shi, S., Yang, B."miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling". Molecular Medicine Reports 19.6 (2019): 5345-5352.
Chicago
Qu, C., Liu, X., Ye, T., Wang, L., Liu, S., Zhou, X., Wu, G., Lin, J., Shi, S., Yang, B."miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling". Molecular Medicine Reports 19, no. 6 (2019): 5345-5352. https://doi.org/10.3892/mmr.2019.10200
Copy and paste a formatted citation
x
Spandidos Publications style
Qu C, Liu X, Ye T, Wang L, Liu S, Zhou X, Wu G, Lin J, Shi S, Yang B, Yang B, et al: miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling. Mol Med Rep 19: 5345-5352, 2019.
APA
Qu, C., Liu, X., Ye, T., Wang, L., Liu, S., Zhou, X. ... Yang, B. (2019). miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling. Molecular Medicine Reports, 19, 5345-5352. https://doi.org/10.3892/mmr.2019.10200
MLA
Qu, C., Liu, X., Ye, T., Wang, L., Liu, S., Zhou, X., Wu, G., Lin, J., Shi, S., Yang, B."miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling". Molecular Medicine Reports 19.6 (2019): 5345-5352.
Chicago
Qu, C., Liu, X., Ye, T., Wang, L., Liu, S., Zhou, X., Wu, G., Lin, J., Shi, S., Yang, B."miR‑216a exacerbates TGF‑β‑induced myofibroblast transdifferentiation via PTEN/AKT signaling". Molecular Medicine Reports 19, no. 6 (2019): 5345-5352. https://doi.org/10.3892/mmr.2019.10200
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