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MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts

  • Authors:
    • Kaiyan Xiao
    • Xusong Luo
    • Xiuxia Wang
    • Zhen Gao
  • View Affiliations / Copyright

    Affiliations: Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, P.R. China
    Copyright: © Xiao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1489-1496
    |
    Published online on: February 8, 2017
       https://doi.org/10.3892/mmr.2017.6179
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Abstract

Transforming growth factor-β1 (TGF-β1) and collagen type I (Col-1) serve a critical role in the development and progression of hypertrophic scarring (HS). The present study hypothesized that a post‑translational mechanism of microRNAs (miR) regulated the expression of TGF‑β1 and Col‑1 in HS fibroblasts (HSFBs). A collection of 20 HS tissues was compared with corresponding normal tissues from clinical patients, and the expression of miR‑185 was measured. Using PicTar, TargetScan and miRBase databases, it was identified that miR‑185 may be a regulator of TGF‑β1 and Col‑1 in humans. Based on these hypotheses, the expression of miR‑185, TGF‑β1 and Col‑1 in HS tissues was investigated. The results demonstrated that the expression of miR‑185 was markedly suppressed, and TGF‑β1 and Col‑1 levels were increased, in HS tissues. The expression levels of endogenous miR‑185 negatively correlated with the TGF‑β1 and Col‑1 mRNA levels (Pearson's correlation coefficient r=‑0.674, P<0.01 and r=‑0.590, P<0.01, respectively). In vitro, miR‑185 can regulate TGF‑β1 and Col‑1 through the predicted binding sites in its 3'‑untranslated region. miR‑185 had an effect on cell proliferation and apoptosis, thereby regulating HSFBs growth. In addition, miR‑185 gain‑of‑function decreased TGF‑β1 and Col‑1 protein expression, and miR‑185 loss‑of‑function increased TGF‑β1 and Col‑1 protein expression in HSFBs. In conclusion, overexpressed miR‑185 could inhibit HSFBs growth, and the underlying mechanism was mediated, at least partly, through the suppression of TGF‑β1 and Col‑1 expression. However, above all, miR‑185 might serve as a potential therapeutic approach for the treatment of HS.
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Copy and paste a formatted citation
Spandidos Publications style
Xiao K, Luo X, Wang X and Gao Z: MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts. Mol Med Rep 15: 1489-1496, 2017.
APA
Xiao, K., Luo, X., Wang, X., & Gao, Z. (2017). MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts. Molecular Medicine Reports, 15, 1489-1496. https://doi.org/10.3892/mmr.2017.6179
MLA
Xiao, K., Luo, X., Wang, X., Gao, Z."MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts". Molecular Medicine Reports 15.4 (2017): 1489-1496.
Chicago
Xiao, K., Luo, X., Wang, X., Gao, Z."MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts". Molecular Medicine Reports 15, no. 4 (2017): 1489-1496. https://doi.org/10.3892/mmr.2017.6179
Copy and paste a formatted citation
x
Spandidos Publications style
Xiao K, Luo X, Wang X and Gao Z: MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts. Mol Med Rep 15: 1489-1496, 2017.
APA
Xiao, K., Luo, X., Wang, X., & Gao, Z. (2017). MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts. Molecular Medicine Reports, 15, 1489-1496. https://doi.org/10.3892/mmr.2017.6179
MLA
Xiao, K., Luo, X., Wang, X., Gao, Z."MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts". Molecular Medicine Reports 15.4 (2017): 1489-1496.
Chicago
Xiao, K., Luo, X., Wang, X., Gao, Z."MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts". Molecular Medicine Reports 15, no. 4 (2017): 1489-1496. https://doi.org/10.3892/mmr.2017.6179
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