Abstract
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.
Keywords:
Collagen type 1; Hypertrophic scar; MicroRNA; Plasminogen activator inhibitor-1; Urokinase type plasminogen activator.
Copyright © 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adolescent
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Adult
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Child
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Cicatrix, Hypertrophic / genetics*
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Cicatrix, Hypertrophic / pathology
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Collagen Type I / biosynthesis*
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Extracellular Matrix / genetics
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Extracellular Matrix / metabolism
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Female
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Fibroblasts / metabolism
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Fibroblasts / pathology
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Gene Expression Regulation
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Humans
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Male
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Matrix Metalloproteinase 1 / biosynthesis
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Matrix Metalloproteinase 1 / genetics
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MicroRNAs / biosynthesis*
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MicroRNAs / genetics
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Plasminogen Activator Inhibitor 1 / genetics*
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Plasminogen Activator Inhibitor 1 / metabolism
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Urokinase-Type Plasminogen Activator / genetics*
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Urokinase-Type Plasminogen Activator / metabolism
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Young Adult
Substances
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Collagen Type I
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MIRN10 microRNA, human
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MIrn181 microRNA, human
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MicroRNAs
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Plasminogen Activator Inhibitor 1
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Urokinase-Type Plasminogen Activator
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MMP1 protein, human
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Matrix Metalloproteinase 1