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miR‑96 promotes collagen deposition in keloids by targeting Smad7

  • Authors:
    • Li Chao
    • Zhu Hua‑Yu
    • Bai Wen‑Dong
    • Song Mei
    • Xiao Bin
    • Hu Da‑Hai
    • Liu Yi
  • View Affiliations / Copyright

    Affiliations: Burns and Plastic Surgery Center of People's Liberation Army, Lanzhou General Hospital of Chinese People's Liberation Army, Lanzhou, Gansu 730050, P.R. China, Department of Burns and Cutaneous Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China, Department of Hematology, Urumqi General Hospital of Chinese People's Liberation Army, Urumqi, Xinjiang 830000, P.R. China
    Copyright: © Chao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 773-781
    |
    Published online on: November 23, 2018
       https://doi.org/10.3892/etm.2018.7008
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Abstract

The abnormal upregulation of transforming growth factor‑β (TGF‑β) signaling has been demonstrated to initiate keloid formation and progression. Keloid is a type of benign skin tumor that may occur following sustaining skin injury. microRNA‑96 (miR‑96) serves an important role in the progression of various malignant diseases. Using reverse transcription quantitative polymerase chain reaction (RT‑qPCR), the present study demonstrated that miR‑96 was overexpressed in keloid‑derived fibroblasts (KFs). Luciferase reporter assay revealed mothers against decapentaplegic homolog (Smad)7, which is one of the important inhibitory factors in the TGF‑β pathway, as a direct target of miR‑96. miR‑96 was initially observed to be correlated with the deposition of type I collagen in KFs in vitro. The miR‑96 antagomir, was directly added into the keloid organ culture (OC) to find its significant antifibrotic potential, such as keloid OC shrinkage, exhibited by its dry weight loss and improved dermis architecture, exhibited by Masson's staining. Following miR‑96 antagomir treatment, a reduction in the mRNA and protein expression levels of collagen type I α 1 chain and collagen type 3 α 1 chain within keloid OC tissues was observed. The present study revealed that miR‑96 serves an important role in pathogenic keloid formation, suggesting that miR‑96 antagomir has the potential to prevent keloid progression.
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Copy and paste a formatted citation
Spandidos Publications style
Chao L, Hua‑Yu Z, Wen‑Dong B, Mei S, Bin X, Da‑Hai H and Yi L: miR‑96 promotes collagen deposition in keloids by targeting Smad7. Exp Ther Med 17: 773-781, 2019.
APA
Chao, L., Hua‑Yu, Z., Wen‑Dong, B., Mei, S., Bin, X., Da‑Hai, H., & Yi, L. (2019). miR‑96 promotes collagen deposition in keloids by targeting Smad7. Experimental and Therapeutic Medicine, 17, 773-781. https://doi.org/10.3892/etm.2018.7008
MLA
Chao, L., Hua‑Yu, Z., Wen‑Dong, B., Mei, S., Bin, X., Da‑Hai, H., Yi, L."miR‑96 promotes collagen deposition in keloids by targeting Smad7". Experimental and Therapeutic Medicine 17.1 (2019): 773-781.
Chicago
Chao, L., Hua‑Yu, Z., Wen‑Dong, B., Mei, S., Bin, X., Da‑Hai, H., Yi, L."miR‑96 promotes collagen deposition in keloids by targeting Smad7". Experimental and Therapeutic Medicine 17, no. 1 (2019): 773-781. https://doi.org/10.3892/etm.2018.7008
Copy and paste a formatted citation
x
Spandidos Publications style
Chao L, Hua‑Yu Z, Wen‑Dong B, Mei S, Bin X, Da‑Hai H and Yi L: miR‑96 promotes collagen deposition in keloids by targeting Smad7. Exp Ther Med 17: 773-781, 2019.
APA
Chao, L., Hua‑Yu, Z., Wen‑Dong, B., Mei, S., Bin, X., Da‑Hai, H., & Yi, L. (2019). miR‑96 promotes collagen deposition in keloids by targeting Smad7. Experimental and Therapeutic Medicine, 17, 773-781. https://doi.org/10.3892/etm.2018.7008
MLA
Chao, L., Hua‑Yu, Z., Wen‑Dong, B., Mei, S., Bin, X., Da‑Hai, H., Yi, L."miR‑96 promotes collagen deposition in keloids by targeting Smad7". Experimental and Therapeutic Medicine 17.1 (2019): 773-781.
Chicago
Chao, L., Hua‑Yu, Z., Wen‑Dong, B., Mei, S., Bin, X., Da‑Hai, H., Yi, L."miR‑96 promotes collagen deposition in keloids by targeting Smad7". Experimental and Therapeutic Medicine 17, no. 1 (2019): 773-781. https://doi.org/10.3892/etm.2018.7008
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