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Research Paper|Volume 11, Issue 9|pp 2898—2910

miR-495 inhibits the growth of fibroblasts in hypertrophic scars

Bingyu Guo1, Qiang Hui1, Zhishan Xu1, Peng Chang1, Kai Tao1
  • 1Reconstructive and Plastic Surgery, General Hospital of Northern Theater, PLA, Shenyang, P.R.China
Received: January 25, 2019Accepted: May 5, 2019Published: May 14, 2019
https://doi.org/10.18632/aging.101965

Copyright: Guo et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Noncoding RNAs are known to be importantly involved in a variety physiological and pathophysiolgical processes. Their role in the pathogenesis of hypertrophic scars remains unclear, however. After preliminary screening of the microRNA (miRNA) gene expression profiles, we explored the role of miR-495 in the development of hypertrophic scar by comparing expression of miR-495 and focal adhesion kinase (FAK) between hypertrophic scar and normal skin tissue. We also used 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and annexin V-fluorescein isothiocyanate/propidium iodide assays to assess the effect of miR-495 on the proliferation and apoptosis in human hypertrophic scar fibroblasts. Western blotting and real-time polymerase chain reaction were used to evaluate expression of miR-495, FAK, and related proteins in the FAK pathway. Our findings show that miR-495 inhibits FAK and its downstream mediators in vitro and vivo, and suggest that miR-495 may be a useful therapeutic target for the treatment of hypertrophic scar.