MicroRNA‑18a‑5p represses scar fibroblast proliferation and extracellular matrix deposition through regulating Smad2 expression
- Tianshi Li
- Yiguang Wu
- Dandan Liu
- Lida Zhuang
Affiliations: Department of Plastic and Cosmetic Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036, P.R. China, Department of Food Science and Engineering, College of Chemistry and Environmental Engineering, Shenzhen University Xili Campus, Shenzhen, Guangdong 518060, P.R. China
- Published online on: September 20, 2021 https://doi.org/10.3892/etm.2021.10753
Copyright: © Li
et al. This is an open access article distributed under the
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The aim of the present study was to investigate the expression and role of microRNA‑18a‑5p (miR‑18a‑5p) during the formation of hypertrophic scar (HS), and to further explore the molecular mechanisms involved. Downregulation of miR‑18a‑5p in HS tissues and human HS fibroblasts (hHSFs) was detected by reverse transcription‑quantitative polymerase chain reaction. The binding sites between miR‑18a‑5p and the 3'‑untranslated region of SMAD family member 2 (Smad2) were predicted by TargetScan and confirmed by dual‑luciferase reporter assay. To investigate the role of miR‑18a‑5p in HS formation, the effects of miR‑18a‑5p downregulation or upregulation on hHSFs were subsequently determined. Cell proliferation was detected by an MTT assay, while cell apoptosis was measured by flow cytometry. In addition, the protein expression levels of Smad2, Collagen I (Col I) and Col III were examined by western blot assay. The findings indicated that miR‑18a‑5p downregulation in hHSFs significantly promoted the cell proliferation, decreased cell apoptosis and enhanced the expression levels of Smad2, Col I and Col III protein and mRNA, whereas miR‑18a‑5p upregulation in hHSFs exerted opposite effects. Notably, the effects of miR‑18a‑5p upregulation on hHSFs were eliminated by Smad2 upregulation. In conclusion, the data indicated that miR‑18a‑5p was downregulated during HS formation, and its upregulation repressed scar fibroblast proliferation and extracellular matrix deposition by targeting Smad2. Therefore, miR‑18a‑5p may serve as a novel therapeutic target for the treatment of HS.