Overexpression of miR-200b inhibits the cell proliferation and promotes apoptosis of human hypertrophic scar fibroblasts in vitro

被引:82
作者
Li, Ping [1 ]
He, Quan-Yong [1 ]
Luo, Cheng-Qun [1 ]
机构
[1] Cent S Univ, Xiang Ya Hosp 3, Dept Plast Surg, Changsha 410013, Hunan, Peoples R China
关键词
collagen; hypertrophic scarring; in vitro; miRNA-200b; TGF-1; alpha-SMA; KELOID FIBROBLASTS; EXPRESSION; GROWTH; TISSUE; MICRORNAS; THERAPY; CANCER; SKIN; DISEASE;
D O I
10.1111/1346-8138.12600
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100227 [皮肤病学];
摘要
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-1/-SMA signaling. Thus, our study provides evidence to support that miR-200b may be a useful target for hypertrophic scarring management.
引用
收藏
页码:903 / 911
页数:9
相关论文
共 30 条
[1]
Enhanced expression of caspase-3 in hypertrophic scars and keloid: Induction of caspase-3 and apoptosis in keloid fibroblasts in vitro [J].
Akasaka, Y ;
Ishikawa, Y ;
Ono, I ;
Fujita, K ;
Masuda, T ;
Asuwa, N ;
Inuzuka, K ;
Kiguchi, H ;
Ishii, T .
LABORATORY INVESTIGATION, 2000, 80 (03) :345-357
[2]
[Anonymous], J AM ACAD DERMATOL
[3]
Site-Specific Keloid Fibroblasts Alter the Behaviour of Normal Skin and Normal Scar Fibroblasts through Paracrine Signalling [J].
Ashcroft, Kevin J. ;
Syed, Farhatullah ;
Bayat, Ardeshir .
PLOS ONE, 2013, 8 (12)
[4]
Bayat Ardeshir, 2005, Skinmed, V4, P165, DOI 10.1111/j.1540-9740.2005.02507.x
[5]
MicroRNA Profiling in Mid- and Late-Gestational Fetal Skin: Implication for Scarless Wound Healing [J].
Cheng, Jie ;
Yu, Hongbo ;
Deng, Simin ;
Shen, Guofang .
TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE, 2010, 221 (03) :203-209
[6]
Differential expression of transforming growth factor-β receptors I and II and activation of Smad 3 in keloid fibroblasts [J].
Chin, GS ;
Liu, W ;
Peled, Z ;
Lee, TY ;
Steinbrech, DS ;
Hsu, M ;
Longaker, MT .
PLASTIC AND RECONSTRUCTIVE SURGERY, 2001, 108 (02) :423-429
[7]
Novel antisense oligonucleotides targeting TGF-β inhibit in vivo scarring and improve surgical outcome [J].
Cordeiro, MF ;
Mead, A ;
Ali, RR ;
Alexander, RA ;
Murray, S ;
Chen, C ;
York-Defalco, C ;
Dean, NM ;
Schultz, GS ;
Khaw, PT .
GENE THERAPY, 2003, 10 (01) :59-71
[8]
TGF-β-induced fibrosis and SMAD signaling:: oligo decoys as natural therapeutics for inhibition of tissue fibrosis and scarring [J].
Cutroneo, Kenneth R. .
WOUND REPAIR AND REGENERATION, 2007, 15 :S54-S60
[9]
MicroRNAs: recently discovered key regulators of proliferation and apoptosis in animal cells - Identification of miRNAs regulating growth and survival [J].
Gammell, Patrick .
CYTOTECHNOLOGY, 2007, 53 (1-3) :55-63
[10]
Hypertrophic Scarring and Keloids: Pathomechanisms and Current and Emerging Treatment Strategies [J].
Gauglitz, Gerd G. ;
Korting, Hans C. ;
Pavicic, Tatiana ;
Ruzicka, Thomas ;
Jeschke, Marc G. .
MOLECULAR MEDICINE, 2011, 17 (1-2) :113-125