Publication Date:
2014-12-31
Description:
Publication date: Available online 29 December 2014 Source: FEBS Letters Author(s): Chao Li , Hua-Yu Zhu , Wen-Dong Bai , Lin-Lin Su , Jia-Qi Liu , Wei-Xia Cai , Bin Zhao , Jian-Xin Gao , Shi-Chao Han , Jun Li , Da-Hai Hu 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 differentially-expressed 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.
Print ISSN:
0014-5793
Electronic ISSN:
1873-3468
Topics:
Biology
,
Chemistry and Pharmacology
,
Physics
