Phenotypic overlap between MMP-13 and the plasminogen activation system during wound healing in mice

Anna Juncker-Jensen; Leif Røge Lund

doi:10.1371/journal.pone.0016954

Phenotypic overlap between MMP-13 and the plasminogen activation system during wound healing in mice

Anna Juncker-Jensen, Leif Røge Lund

26 Citations (Scopus)

Abstract

Proteolytic degradation of extracellular matrix is a crucial step in the healing of incisional skin wounds. Thus, healing of skin wounds is delayed by either plasminogen-deficiency or by treatment with the broad-spectrum metalloproteinase (MP) inhibitor Galardin alone, while the two perturbations combined completely prevent wound healing. Both urokinase-type plasminogen activator and several matrix metallo proteinases (MMPs), such as MMP-3, -9 and -13, are expressed in the leading-edge keratinocytes of skin wounds, which may account for this phenotypic overlap between these classes of proteases.

Original language	English
Journal	P L o S One
Volume	6
Issue number	2
Pages (from-to)	e16954
ISSN	1932-6203
DOIs	https://doi.org/10.1371/journal.pone.0016954
Publication status	Published - 2011

Keywords

Animals
Female
Male
Matrix Metalloproteinase 13
Mice
Mice, Knockout
Phenotype
Plasminogen
Plasminogen Activators
Pregnancy
Signal Transduction
Skin Diseases
Survival
Urokinase-Type Plasminogen Activator
Wound Healing

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10.1371/journal.pone.0016954

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title = "Phenotypic overlap between MMP-13 and the plasminogen activation system during wound healing in mice",

abstract = "Proteolytic degradation of extracellular matrix is a crucial step in the healing of incisional skin wounds. Thus, healing of skin wounds is delayed by either plasminogen-deficiency or by treatment with the broad-spectrum metalloproteinase (MP) inhibitor Galardin alone, while the two perturbations combined completely prevent wound healing. Both urokinase-type plasminogen activator and several matrix metallo proteinases (MMPs), such as MMP-3, -9 and -13, are expressed in the leading-edge keratinocytes of skin wounds, which may account for this phenotypic overlap between these classes of proteases.",

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journal = "P L o S One",

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T1 - Phenotypic overlap between MMP-13 and the plasminogen activation system during wound healing in mice

AU - Juncker-Jensen, Anna

AU - Lund, Leif Røge

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N2 - Proteolytic degradation of extracellular matrix is a crucial step in the healing of incisional skin wounds. Thus, healing of skin wounds is delayed by either plasminogen-deficiency or by treatment with the broad-spectrum metalloproteinase (MP) inhibitor Galardin alone, while the two perturbations combined completely prevent wound healing. Both urokinase-type plasminogen activator and several matrix metallo proteinases (MMPs), such as MMP-3, -9 and -13, are expressed in the leading-edge keratinocytes of skin wounds, which may account for this phenotypic overlap between these classes of proteases.

AB - Proteolytic degradation of extracellular matrix is a crucial step in the healing of incisional skin wounds. Thus, healing of skin wounds is delayed by either plasminogen-deficiency or by treatment with the broad-spectrum metalloproteinase (MP) inhibitor Galardin alone, while the two perturbations combined completely prevent wound healing. Both urokinase-type plasminogen activator and several matrix metallo proteinases (MMPs), such as MMP-3, -9 and -13, are expressed in the leading-edge keratinocytes of skin wounds, which may account for this phenotypic overlap between these classes of proteases.

KW - Animals

KW - Female

KW - Male

KW - Matrix Metalloproteinase 13

KW - Mice

KW - Mice, Knockout

KW - Phenotype

KW - Plasminogen

KW - Plasminogen Activators

KW - Pregnancy

KW - Signal Transduction

KW - Skin Diseases

KW - Survival

KW - Urokinase-Type Plasminogen Activator

KW - Wound Healing

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U2 - 10.1371/journal.pone.0016954

DO - 10.1371/journal.pone.0016954

M3 - Journal article

C2 - 21326869

SN - 1932-6203

VL - 6

SP - e16954

JO - P L o S One

JF - P L o S One

IS - 2

ER -

Phenotypic overlap between MMP-13 and the plasminogen activation system during wound healing in mice

Abstract

Keywords

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