MiR-10a and miR-181c regulate collagen type I generation in hypertrophic scars by targeting PAI-1 and uPA

被引：40

作者：

Li, Chao ^{[1
]}

Zhu, Hua-Yu ^{[1
]}

Bai, Wen-Dong ^{[2
]}

Su, Lin-Lin ^{[1
]}

Liu, Jia-Qi ^{[1
]}

Cai, Wei-Xia ^{[1
]}

Zhao, Bin ^{[1
]}

Gao, Jian-Xin ^{[1
]}

Han, Shi-Chao ^{[1
]}

Li, Jun ^{[1
]}

Hu, Da-Hai ^{[1
]}

机构：

[1] Fourth Mil Med Univ, Xijing Hosp, Dept Burns & Cutaneous Surg, Xian 710032, Shanxi, Peoples R China

[2] Fourth Mil Med Univ, Dept Immunol, Xian 710032, Shanxi, Peoples R China

来源：

FEBS LETTERS | 2015年 / 589卷 / 03期

基金：

中国博士后科学基金;

关键词：

MicroRNA; Hypertrophic scar; Collagen type 1; Urokinase type plasminogen activator; Plasminogen activator inhibitor-1; PLASMINOGEN-ACTIVATOR INHIBITOR-1; DIFFERENTIAL EXPRESSION; LIVER FIBROSIS; III COLLAGEN; MOUSE SKIN; UROKINASE; FIBROBLASTS; MICRORNAS; GROWTH; MIGRATION;

D O I：

10.1016/j.febslet.2014.12.024

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Urokinase type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) have been proposed to play key roles in extracellular matrix (ECM) deposition in hypertrophic scars (HS). Here, we found that in HS fibroblasts (HFs) miR-181c and miR-10a were differentiallyexpressed and targeted uPA and PAI-1, respectively. The production of Type 1 collagen (Col1) was inhibited by miR-181c knockdown or miR-10a overexpression in HFs, and this resulted in increased levels of metalloproteinase 1 (MMP1). These results suggest that the miR-181c-uPA and miR-10a-PAI-1 regulatory pathways have an integral role in HS pathogenesis. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：380 / 389

页数：10

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