Overexpression of miR‐200b inhibits the cell proliferation and promotes apoptosis of human hypertrophic scar fibroblastsin vitro
Ping Li, Quanyong He, Chengqun Luo
Abstract
Ping Li, Quanyong He, Chengqun Luo
Abstract
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 miRNA 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 miRNA microarray. The results of miRNA array showed that miR-200b was downregulated by more than 2-fold, validated by qPCR 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.
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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 miRNA 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 miRNA microarray. The results of miRNA array showed that miR-200b was downregulated by more than 2-fold, validated by qPCR 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.
Key concepts: Hypertrophic scar, Keloid, Fibronectin, Medicine, Apoptosis, microRNA, Pathology, Wound healing