MicroRNA-222 regulates the viability of fibroblasts in hypertrophic scars via matrix metalloproteinase 1
- Yi Zhang
- Xiaohua Lin
- Li Zhang
- Weilong Hong
- Kang Zeng
Published online on: December 14, 2017
Copyright: © Zhang et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
The present study aimed to determine the expression of microRNA (miR)‑222 in hypertrophic scar (HS) tissues, and investigate the regulatory mechanism of miR‑222 in HS. A total of 36 patients diagnosed with HS between August 2013 and May 2016 were included in the present study. HS tissues and HS‑adjacent tissues were collected from patients. Primary fibroblasts were obtained from HS tissue. Reverse transcription‑quantitative polymerase chain reaction was used to measure mRNA levels of matrix metalloproteinase 1 (MMP1) and miR‑222. Western blotting was conducted to determine MMP1 expression and an MTT assay was performed to measure the viability of fibroblasts. A dual luciferase reporter assay was used to identify the binding of miR‑222 to MMP1 mRNA. It was demonstrated that MMP1 serves a role in HS at the transcription level and that increased MMP1 expression inhibited the viability of fibroblasts. miR‑222 serves a regulatory role in HS by targeting its target gene MMP1 and regulates the expression of MMP1 by binding to its 3'‑untranslated region. The decreased expression of miR‑222 suppresses the viability of fibroblasts by regulating MMP1 expression. The present study demonstrated that the downregulation of MMP1 in HS tissues is associated with the upregulation of miR‑222 expression. miR‑222 may therefore regulate the viability of fibroblasts in HS and the expression of related proteins via MMP1.