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Overexpression of miR‐200b inhibits the cell proliferation and promotes apoptosis of human hypertrophic scar fibroblasts in vitro
Author(s) -
Li Ping,
He QuanYong,
Luo ChengQun
Publication year - 2014
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/1346-8138.12600
Subject(s) - hypertrophic scar , keloid , fibronectin , microrna , apoptosis , medicine , cell growth , wound healing , cell , muscle hypertrophy , pathology , microbiology and biotechnology , biology , immunology , extracellular matrix , gene , genetics
Hypertrophic scarring leads to a deformed appearance and contracted neogenetic tissue, resulting in physiological and psychological problems for patients. Millions of people suffer these discomforts each year. Emerging evidence has reported that mi RNA contributed to hypertrophic scarring or keloid formation. In this study, nine hypertrophic scar samples and the matched normal skin tissues were used to perform a mi RNA microarray. The results of mi RNA array showed that miR‐200b was downregulated by more than 2‐fold, validated by q PCR in hypertrophic scar tissues and human hypertrophic scar fibroblasts, suggesting that there was an important correlation between miR‐200b and hypertrophic scarring. We also found that miR‐200b affected hypertrophic scarring through regulating the cell proliferation and apoptosis of human hypertrophic scar fibroblasts by affecting the collagen I and III synthesis, fibronectin expression and TGF ‐β1/α‐ SMA signaling. Thus, our study provides evidence to support that miR‐200b may be a useful target for hypertrophic scarring management.