Granzyme B mediates both direct and indirect cleavage of extracellular matrix in skin after chronic low-dose ultraviolet light irradiation.
Identifieur interne : 000566 ( PubMed/Curation ); précédent : 000565; suivant : 000567Granzyme B mediates both direct and indirect cleavage of extracellular matrix in skin after chronic low-dose ultraviolet light irradiation.
Auteurs : Leigh G. Parkinson [Canada] ; Ana Toro ; Hongyan Zhao ; Keddie Brown ; Scott J. Tebbutt ; David J. GranvilleSource :
- Aging cell [ 1474-9726 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Cell Count, Collagen (metabolism), Decorin (metabolism), Dermis (pathology), Dermis (radiation effects), Dose-Response Relationship, Radiation, Extracellular Matrix (metabolism), Female, Fibroblasts (enzymology), Fibroblasts (radiation effects), Fibronectins (metabolism), Granzymes (deficiency), Granzymes (metabolism), Mast Cells (enzymology), Mast Cells (radiation effects), Matrix Metalloproteinase 1 (metabolism), Mice, Inbred C57BL, Mice, Knockout, Models, Biological, Protein Transport (radiation effects), Proteolysis (radiation effects), Skin (metabolism), Skin (radiation effects), Skin Aging (radiation effects), Ultraviolet Rays.
- MESH :
- chemical , deficiency : Granzymes.
- chemical , metabolism : Collagen, Decorin, Fibronectins, Granzymes, Matrix Metalloproteinase 1.
- enzymology : Fibroblasts, Mast Cells.
- metabolism : Extracellular Matrix, Skin.
- pathology : Dermis.
- radiation effects : Dermis, Fibroblasts, Mast Cells, Protein Transport, Proteolysis, Skin, Skin Aging.
- Animals, Cell Count, Dose-Response Relationship, Radiation, Female, Mice, Inbred C57BL, Mice, Knockout, Models, Biological, Ultraviolet Rays.
Abstract
Extracellular matrix (ECM) degradation is a hallmark of many chronic inflammatory diseases that can lead to a loss of function, aging, and disease progression. Ultraviolet light (UV) irradiation from the sun is widely considered as the major cause of visible human skin aging, causing increased inflammation and enhanced ECM degradation. Granzyme B (GzmB), a serine protease that is expressed by a variety of cells, accumulates in the extracellular milieu during chronic inflammation and cleaves a number of ECM proteins. We hypothesized that GzmB contributes to ECM degradation in the skin after UV irradiation through both direct cleavage of ECM proteins and indirectly through the induction of other proteinases. Wild-type and GzmB-knockout mice were repeatedly exposed to minimal erythemal doses of solar-simulated UV irradiation for 20 weeks. GzmB expression was significantly increased in wild-type treated skin compared to nonirradiated controls, colocalizing to keratinocytes and to an increased mast cell population. GzmB deficiency significantly protected against the formation of wrinkles and the loss of dermal collagen density, which was related to the cleavage of decorin, an abundant proteoglycan involved in collagen fibrillogenesis and integrity. GzmB also cleaved fibronectin, and GzmB-mediated fibronectin fragments increased the expression of collagen-degrading matrix metalloproteinase-1 (MMP-1) in fibroblasts. Collectively, these findings indicate a significant role for GzmB in ECM degradation that may have implications in many age-related chronic inflammatory diseases.
DOI: 10.1111/acel.12298
PubMed: 25495009
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pubmed:25495009Le document en format XML
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<series><title level="j">Aging cell</title>
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<term>Cell Count</term>
<term>Collagen (metabolism)</term>
<term>Decorin (metabolism)</term>
<term>Dermis (pathology)</term>
<term>Dermis (radiation effects)</term>
<term>Dose-Response Relationship, Radiation</term>
<term>Extracellular Matrix (metabolism)</term>
<term>Female</term>
<term>Fibroblasts (enzymology)</term>
<term>Fibroblasts (radiation effects)</term>
<term>Fibronectins (metabolism)</term>
<term>Granzymes (deficiency)</term>
<term>Granzymes (metabolism)</term>
<term>Mast Cells (enzymology)</term>
<term>Mast Cells (radiation effects)</term>
<term>Matrix Metalloproteinase 1 (metabolism)</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Models, Biological</term>
<term>Protein Transport (radiation effects)</term>
<term>Proteolysis (radiation effects)</term>
<term>Skin (metabolism)</term>
<term>Skin (radiation effects)</term>
<term>Skin Aging (radiation effects)</term>
<term>Ultraviolet Rays</term>
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<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Granzymes</term>
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<term>Decorin</term>
<term>Fibronectins</term>
<term>Granzymes</term>
<term>Matrix Metalloproteinase 1</term>
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<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Fibroblasts</term>
<term>Mast Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Extracellular Matrix</term>
<term>Skin</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dermis</term>
</keywords>
<keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Dermis</term>
<term>Fibroblasts</term>
<term>Mast Cells</term>
<term>Protein Transport</term>
<term>Proteolysis</term>
<term>Skin</term>
<term>Skin Aging</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Count</term>
<term>Dose-Response Relationship, Radiation</term>
<term>Female</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Models, Biological</term>
<term>Ultraviolet Rays</term>
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<front><div type="abstract" xml:lang="en">Extracellular matrix (ECM) degradation is a hallmark of many chronic inflammatory diseases that can lead to a loss of function, aging, and disease progression. Ultraviolet light (UV) irradiation from the sun is widely considered as the major cause of visible human skin aging, causing increased inflammation and enhanced ECM degradation. Granzyme B (GzmB), a serine protease that is expressed by a variety of cells, accumulates in the extracellular milieu during chronic inflammation and cleaves a number of ECM proteins. We hypothesized that GzmB contributes to ECM degradation in the skin after UV irradiation through both direct cleavage of ECM proteins and indirectly through the induction of other proteinases. Wild-type and GzmB-knockout mice were repeatedly exposed to minimal erythemal doses of solar-simulated UV irradiation for 20 weeks. GzmB expression was significantly increased in wild-type treated skin compared to nonirradiated controls, colocalizing to keratinocytes and to an increased mast cell population. GzmB deficiency significantly protected against the formation of wrinkles and the loss of dermal collagen density, which was related to the cleavage of decorin, an abundant proteoglycan involved in collagen fibrillogenesis and integrity. GzmB also cleaved fibronectin, and GzmB-mediated fibronectin fragments increased the expression of collagen-degrading matrix metalloproteinase-1 (MMP-1) in fibroblasts. Collectively, these findings indicate a significant role for GzmB in ECM degradation that may have implications in many age-related chronic inflammatory diseases.</div>
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<Abstract><AbstractText>Extracellular matrix (ECM) degradation is a hallmark of many chronic inflammatory diseases that can lead to a loss of function, aging, and disease progression. Ultraviolet light (UV) irradiation from the sun is widely considered as the major cause of visible human skin aging, causing increased inflammation and enhanced ECM degradation. Granzyme B (GzmB), a serine protease that is expressed by a variety of cells, accumulates in the extracellular milieu during chronic inflammation and cleaves a number of ECM proteins. We hypothesized that GzmB contributes to ECM degradation in the skin after UV irradiation through both direct cleavage of ECM proteins and indirectly through the induction of other proteinases. Wild-type and GzmB-knockout mice were repeatedly exposed to minimal erythemal doses of solar-simulated UV irradiation for 20 weeks. GzmB expression was significantly increased in wild-type treated skin compared to nonirradiated controls, colocalizing to keratinocytes and to an increased mast cell population. GzmB deficiency significantly protected against the formation of wrinkles and the loss of dermal collagen density, which was related to the cleavage of decorin, an abundant proteoglycan involved in collagen fibrillogenesis and integrity. GzmB also cleaved fibronectin, and GzmB-mediated fibronectin fragments increased the expression of collagen-degrading matrix metalloproteinase-1 (MMP-1) in fibroblasts. Collectively, these findings indicate a significant role for GzmB in ECM degradation that may have implications in many age-related chronic inflammatory diseases.</AbstractText>
<CopyrightInformation>© 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.</CopyrightInformation>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D008407" MajorTopicYN="N">Mast Cells</DescriptorName>
<QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName>
<QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020781" MajorTopicYN="N">Matrix Metalloproteinase 1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D021381" MajorTopicYN="N">Protein Transport</DescriptorName>
<QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059748" MajorTopicYN="N">Proteolysis</DescriptorName>
<QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012867" MajorTopicYN="N">Skin</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000528" MajorTopicYN="Y">radiation effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015595" MajorTopicYN="N">Skin Aging</DescriptorName>
<QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014466" MajorTopicYN="Y">Ultraviolet Rays</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<OtherID Source="NLM">PMC4326907</OtherID>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">aging</Keyword>
<Keyword MajorTopicYN="N">collagen</Keyword>
<Keyword MajorTopicYN="N">extracellular matrix</Keyword>
<Keyword MajorTopicYN="N">fibronectin</Keyword>
<Keyword MajorTopicYN="N">granzyme B</Keyword>
<Keyword MajorTopicYN="N">matrix metalloproteinase</Keyword>
<Keyword MajorTopicYN="N">photoaging</Keyword>
<Keyword MajorTopicYN="N">skin</Keyword>
<Keyword MajorTopicYN="N">ultraviolet light</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2014</Year>
<Month>11</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2014</Year>
<Month>12</Month>
<Day>16</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2014</Year>
<Month>12</Month>
<Day>17</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2015</Year>
<Month>9</Month>
<Day>29</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">25495009</ArticleId>
<ArticleId IdType="doi">10.1111/acel.12298</ArticleId>
<ArticleId IdType="pmc">PMC4326907</ArticleId>
</ArticleIdList>
</PubmedData>
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