Delayed reepithelialization and basement membrane regeneration after wounding in mice lacking CXCR3
Identifieur interne : 001C19 ( Istex/Corpus ); précédent : 001C18; suivant : 001C20Delayed reepithelialization and basement membrane regeneration after wounding in mice lacking CXCR3
Auteurs : Cecelia C. Yates ; Diana Whaley ; Shveta Hooda ; Patricia A. Hebda ; Richard J. Bodnar ; Alan WellsSource :
- Wound Repair and Regeneration [ 1067-1927 ] ; 2009-01.
English descriptors
- KwdEn :
- Amino receptor, Basement membrane, Basement membrane components, Broblasts, Cell biol, Cell motility, Chemokine, Collagen, Cutaneous wound healing, Cxcr3, Cxcr3 ligands, Cytokeratin, Days postwounding, Dermal, Dermal maturation, Dermis, Epidermal, Epidermal maturation, Epidermis, Epithelial, Epithelial repair, Healing, Investig dermatol, Keratinocyte, Keratinocytes, Ligand, Matrix, Maturation, Membrane, Motility, Mouse, Photomicrograph, Photomicrographs measure, Photomicrographs measures, Polyclonal, Postwounding, Provisional matrix, Rabbit polyclonal, Receptor, Reepithelialization, Regenerative phase, Same time, Wound biopsies, Wound healing, Wound healing society yates, Wound repair, Wound repair regen, Yates.
- Teeft :
- Amino receptor, Basement membrane, Basement membrane components, Broblasts, Cell biol, Cell motility, Chemokine, Collagen, Cutaneous wound healing, Cxcr3, Cxcr3 ligands, Cytokeratin, Days postwounding, Dermal, Dermal maturation, Dermis, Epidermal, Epidermal maturation, Epidermis, Epithelial, Epithelial repair, Healing, Investig dermatol, Keratinocyte, Keratinocytes, Ligand, Matrix, Maturation, Membrane, Motility, Mouse, Photomicrograph, Photomicrographs measure, Photomicrographs measures, Polyclonal, Postwounding, Provisional matrix, Rabbit polyclonal, Receptor, Reepithelialization, Regenerative phase, Same time, Wound biopsies, Wound healing, Wound healing society yates, Wound repair, Wound repair regen, Yates.
Abstract
Wound healing is a complex, orchestrated series of biological events that is controlled by extracellular components that communicate between cell types to re‐establish lost tissue. We have found that signaling by ELR‐negative CXC chemokines through their common CXCR3 receptor is critical for dermal maturation during the resolving phase. In addition there needs to be complete maturation of the epidermis and regeneration of a delineating basement membrane for proper functioning. The role of this ligand–receptor system appears confounding as one ligand, CXCL4/(PF4), is present during the initial dissolution and two others, CXCL10/(IP‐10) and CXCL11/(IP‐9/I‐TAC), are expressed by keratinocytes in the later regenerative and resolving phases during which the basement membrane is re‐established. We examined CXCR3 signaling role in healing using a mouse lacking this receptor, as all three ligands act solely via the common receptor. Reepithelialization was delayed in CXCR3‐deficient mice in both full and partial‐thickness excisional wounds. Even at 90 days postwounding, the epidermis of these mice appeared less mature with lower levels of E‐cadherin and cytokeratin 18. The underlying basement membrane, a product of both dermal fibroblasts and epidermal keratinocytes, was not fully established with persistent diffuse expression of the matrix components laminin 5, collagen IV, and collagen VII throughout the wound bed. These results suggest that CXCR3 and its ligands play an important role in the re‐establishment of the basement membrane and epidermis. These studies further establish the emerging signaling network that involves the CXCR3 chemokine receptor and its ligands as a key regulator of wound repair.
Url:
DOI: 10.1111/j.1524-475X.2008.00439.x
Links to Exploration step
ISTEX:796A25BFC05828B48A6CD9861AD088B3B8B85F79Le document en format XML
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We have found that signaling by ELR‐negative CXC chemokines through their common CXCR3 receptor is critical for dermal maturation during the resolving phase. In addition there needs to be complete maturation of the epidermis and regeneration of a delineating basement membrane for proper functioning. The role of this ligand–receptor system appears confounding as one ligand, CXCL4/(PF4), is present during the initial dissolution and two others, CXCL10/(IP‐10) and CXCL11/(IP‐9/I‐TAC), are expressed by keratinocytes in the later regenerative and resolving phases during which the basement membrane is re‐established. We examined CXCR3 signaling role in healing using a mouse lacking this receptor, as all three ligands act solely via the common receptor. Reepithelialization was delayed in CXCR3‐deficient mice in both full and partial‐thickness excisional wounds. Even at 90 days postwounding, the epidermis of these mice appeared less mature with lower levels of E‐cadherin and cytokeratin 18. The underlying basement membrane, a product of both dermal fibroblasts and epidermal keratinocytes, was not fully established with persistent diffuse expression of the matrix components laminin 5, collagen IV, and collagen VII throughout the wound bed. These results suggest that CXCR3 and its ligands play an important role in the re‐establishment of the basement membrane and epidermis. These studies further establish the emerging signaling network that involves the CXCR3 chemokine receptor and its ligands as a key regulator of wound repair.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>cxcr3</json:string><json:string>epidermal</json:string><json:string>keratinocytes</json:string><json:string>receptor</json:string><json:string>reepithelialization</json:string><json:string>dermis</json:string><json:string>basement membrane</json:string><json:string>keratinocyte</json:string><json:string>postwounding</json:string><json:string>epithelial</json:string><json:string>motility</json:string><json:string>epidermal maturation</json:string><json:string>cytokeratin</json:string><json:string>yates</json:string><json:string>polyclonal</json:string><json:string>broblasts</json:string><json:string>dermal</json:string><json:string>days postwounding</json:string><json:string>rabbit polyclonal</json:string><json:string>epidermis</json:string><json:string>wound healing</json:string><json:string>wound repair</json:string><json:string>chemokine</json:string><json:string>matrix</json:string><json:string>epithelial repair</json:string><json:string>maturation</json:string><json:string>ligand</json:string><json:string>photomicrograph</json:string><json:string>amino receptor</json:string><json:string>dermal maturation</json:string><json:string>wound healing society yates</json:string><json:string>same time</json:string><json:string>wound repair regen</json:string><json:string>regenerative phase</json:string><json:string>wound biopsies</json:string><json:string>cutaneous wound healing</json:string><json:string>provisional matrix</json:string><json:string>photomicrographs measure</json:string><json:string>photomicrographs measures</json:string><json:string>cxcr3 ligands</json:string><json:string>cell biol</json:string><json:string>investig dermatol</json:string><json:string>cell motility</json:string><json:string>basement membrane components</json:string><json:string>mouse</json:string><json:string>collagen</json:string><json:string>healing</json:string><json:string>membrane</json:string></teeft></keywords><author><json:item><name>Cecelia C. 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We have found that signaling by ELR‐negative CXC chemokines through their common CXCR3 receptor is critical for dermal maturation during the resolving phase. In addition there needs to be complete maturation of the epidermis and regeneration of a delineating basement membrane for proper functioning. The role of this ligand–receptor system appears confounding as one ligand, CXCL4/(PF4), is present during the initial dissolution and two others, CXCL10/(IP‐10) and CXCL11/(IP‐9/I‐TAC), are expressed by keratinocytes in the later regenerative and resolving phases during which the basement membrane is re‐established. We examined CXCR3 signaling role in healing using a mouse lacking this receptor, as all three ligands act solely via the common receptor. Reepithelialization was delayed in CXCR3‐deficient mice in both full and partial‐thickness excisional wounds. Even at 90 days postwounding, the epidermis of these mice appeared less mature with lower levels of E‐cadherin and cytokeratin 18. The underlying basement membrane, a product of both dermal fibroblasts and epidermal keratinocytes, was not fully established with persistent diffuse expression of the matrix components laminin 5, collagen IV, and collagen VII throughout the wound bed. These results suggest that CXCR3 and its ligands play an important role in the re‐establishment of the basement membrane and epidermis. These studies further establish the emerging signaling network that involves the CXCR3 chemokine receptor and its ligands as a key regulator of wound repair.</abstract><qualityIndicators><score>9.875</score><pdfWordCount>4887</pdfWordCount><pdfCharCount>30979</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>593.972 x 782.986 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>249</abstractWordCount><abstractCharCount>1725</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Delayed reepithelialization and basement membrane regeneration after wounding in mice lacking CXCR3</title><pmid><json:string>19152649</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Wound Repair and Regeneration</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1524-475X</json:string></doi><issn><json:string>1067-1927</json:string></issn><eissn><json:string>1524-475X</json:string></eissn><publisherId><json:string>WRR</json:string></publisherId><volume>17</volume><issue>1</issue><pages><first>34</first><last>41</last><total>8</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2009</json:string></date><geogName></geogName><orgName><json:string>Affair Medical Center, Pittsburgh</json:string><json:string>Sefar Filtration Inc.</json:string><json:string>University of Pittsburgh</json:string><json:string>Laboratory Animal Care</json:string><json:string>Vector Laboratories</json:string><json:string>D Systems, Minneapolis</json:string><json:string>Universal Imaging Corp.</json:string><json:string>Santa Cruz Biotechnology</json:string><json:string>Pittsburgh VA Medical Center</json:string><json:string>Medtech, Jackson</json:string><json:string>Bio-Rad Laboratories</json:string><json:string>Perlmutter Laboratory, Children</json:string><json:string>Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania Reprint</json:string><json:string>Tuskegee University Carver Research Foundation, Tuskegee, Alabama</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Diana Whaley</json:string><json:string>Alan Wells</json:string><json:string>Diane George</json:string><json:string>Richard J. 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CXCR3</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><availability><licence>© 2009 by the Wound Healing Society</licence></availability><date type="published" when="2009-01"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Delayed reepithelialization and basement membrane regeneration after wounding in mice lacking CXCR3</title><title level="a" type="short">Deficient epithelial repair in CXCR3−/− mice</title><author xml:id="author-0000"><persName><forename type="first">Cecelia C.</forename><surname>Yates</surname><roleName type="degree">BS</roleName></persName><affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania,<address><country key="US"></country></address></affiliation><affiliation>Pittsburgh VAMC, Pittsburgh, Pennsylvania,<address><country key="US"></country></address></affiliation><affiliation>Tuskegee University Carver Research Foundation, Tuskegee, Alabama, and<address><country key="US"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Diana</forename><surname>Whaley</surname><roleName type="degree">MS</roleName></persName><affiliation>Pittsburgh VAMC, Pittsburgh, Pennsylvania,<address><country key="US"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Shveta</forename><surname>Hooda</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania,<address><country key="US"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Patricia A.</forename><surname>Hebda</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania<address><country key="US"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Richard J.</forename><surname>Bodnar</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania,<address><country key="US"></country></address></affiliation><affiliation>Pittsburgh VAMC, Pittsburgh, Pennsylvania,<address><country key="US"></country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Alan</forename><surname>Wells</surname><roleName type="degree">MD, DMSc</roleName></persName><affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania,<address><country key="US"></country></address></affiliation><affiliation>Pittsburgh VAMC, Pittsburgh, Pennsylvania,<address><country key="US"></country></address></affiliation><affiliation>Tuskegee University Carver Research Foundation, Tuskegee, Alabama, and<address><country key="US"></country></address></affiliation></author><idno type="istex">796A25BFC05828B48A6CD9861AD088B3B8B85F79</idno><idno type="ark">ark:/67375/WNG-7J87D5Q8-H</idno><idno type="DOI">10.1111/j.1524-475X.2008.00439.x</idno><idno type="unit">WRR439</idno><idno type="supplier">439</idno><idno type="toTypesetVersion">file:WRR.WRR439.pdf</idno></analytic><monogr><title level="j" type="main">Wound Repair and Regeneration</title><title level="j" type="alt">WOUND REPAIR REGENERATION</title><idno type="pISSN">1067-1927</idno><idno type="eISSN">1524-475X</idno><idno type="book-DOI">10.1111/(ISSN)1524-475X</idno><idno type="book-part-DOI">10.1111/wrr.2009.17.issue-1</idno><idno type="product">WRR</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">17</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="34">34</biblScope><biblScope unit="page" to="41">41</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><date type="published" when="2009-01"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>ABSTRACT</head><p>Wound healing is a complex, orchestrated series of biological events that is controlled by extracellular components that communicate between cell types to re‐establish lost tissue. We have found that signaling by ELR‐negative CXC chemokines through their common CXCR3 receptor is critical for dermal maturation during the resolving phase. In addition there needs to be complete maturation of the epidermis and regeneration of a delineating basement membrane for proper functioning. The role of this ligand–receptor system appears confounding as one ligand, CXCL4/(PF4), is present during the initial dissolution and two others, CXCL10/(IP‐10) and CXCL11/(IP‐9/I‐TAC), are expressed by keratinocytes in the later regenerative and resolving phases during which the basement membrane is re‐established. We examined CXCR3 signaling role in healing using a mouse lacking this receptor, as all three ligands act solely via the common receptor. Reepithelialization was delayed in CXCR3‐deficient mice in both full and partial‐thickness excisional wounds. Even at 90 days postwounding, the epidermis of these mice appeared less mature with lower levels of E‐cadherin and cytokeratin 18. The underlying basement membrane, a product of both dermal fibroblasts and epidermal keratinocytes, was not fully established with persistent diffuse expression of the matrix components laminin 5, collagen IV, and collagen VII throughout the wound bed. These results suggest that CXCR3 and its ligands play an important role in the re‐establishment of the basement membrane and epidermis. These studies further establish the emerging signaling network that involves the CXCR3 chemokine receptor and its ligands as a key regulator of wound repair.</p></abstract><textClass><keywords rend="tocHeading1"><term>Original Research – Basic Science</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/796A25BFC05828B48A6CD9861AD088B3B8B85F79/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Inc</publisherName><publisherLoc>Malden, USA</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1524-475X</doi><issn type="print">1067-1927</issn><issn type="electronic">1524-475X</issn><idGroup><id type="product" value="WRR"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="WOUND REPAIR REGENERATION">Wound Repair and Regeneration</title></titleGroup></publicationMeta><publicationMeta level="part" position="01001"><doi origin="wiley">10.1111/wrr.2009.17.issue-1</doi><numberingGroup><numbering type="journalVolume" number="17">17</numbering><numbering type="journalIssue" number="1">1</numbering></numberingGroup><coverDate startDate="2009-01">January/February 2009</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="4" status="forIssue"><doi origin="wiley">10.1111/j.1524-475X.2008.00439.x</doi><idGroup><id type="unit" value="WRR439"></id><id type="supplier" value="439"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">Original Research – Basic Science</title></titleGroup><copyright>© 2009 by the Wound Healing Society</copyright><eventGroup><event type="firstOnline" date="2009-01-16"></event><event type="publishedOnlineFinalForm" date="2009-01-16"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-02"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-10"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-04"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="34">34</numbering><numbering type="pageLast" number="41">41</numbering></numberingGroup><correspondenceTo><b>Reprint requests:</b>
Alan Wells, MD, DMSc, Department of Pathology, University of Pittsburgh, 3550 Terrace St. Scaife Hall, S‐713 Pittsburgh, PA 15261.
Tel: +1 412 647 7813;
Fax: +1 412 647 8567;
Email: <email normalForm="wellsa@upmc.edu">wellsa@upmc.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:WRR.WRR439.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Manuscript received: December 5, 2007Accepted in final form: June 30, 2008</unparsedEditorialHistory><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="20"></count><count type="wordTotal" number="5628"></count><count type="linksCrossRef" number="57"></count></countGroup><titleGroup><title type="main">Delayed reepithelialization and basement membrane regeneration after wounding in mice lacking CXCR3</title><title type="shortAuthors">Yates et al.</title><title type="short">Deficient epithelial repair in CXCR3−/− mice</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2 #a3"><personName><givenNames>Cecelia C.</givenNames><familyName>Yates</familyName><degrees>BS</degrees></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>Diana</givenNames><familyName>Whaley</familyName><degrees>MS</degrees></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Shveta</givenNames><familyName>Hooda</familyName><degrees>MD</degrees></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a4"><personName><givenNames>Patricia A.</givenNames><familyName>Hebda</familyName><degrees>PhD</degrees></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1 #a2"><personName><givenNames>Richard J.</givenNames><familyName>Bodnar</familyName><degrees>PhD</degrees></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1 #a2 #a3"><personName><givenNames>Alan</givenNames><familyName>Wells</familyName><degrees>MD, DMSc</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania,</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Pittsburgh VAMC, Pittsburgh, Pennsylvania,</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="US"><unparsedAffiliation>Tuskegee University Carver Research Foundation, Tuskegee, Alabama, and</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="US"><unparsedAffiliation>Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">ABSTRACT</title><p>Wound healing is a complex, orchestrated series of biological events that is controlled by extracellular components that communicate between cell types to re‐establish lost tissue. We have found that signaling by ELR‐negative CXC chemokines through their common CXCR3 receptor is critical for dermal maturation during the resolving phase. In addition there needs to be complete maturation of the epidermis and regeneration of a delineating basement membrane for proper functioning. The role of this ligand–receptor system appears confounding as one ligand, CXCL4/(PF4), is present during the initial dissolution and two others, CXCL10/(IP‐10) and CXCL11/(IP‐9/I‐TAC), are expressed by keratinocytes in the later regenerative and resolving phases during which the basement membrane is re‐established. We examined CXCR3 signaling role in healing using a mouse lacking this receptor, as all three ligands act solely via the common receptor. Reepithelialization was delayed in CXCR3‐deficient mice in both full and partial‐thickness excisional wounds. Even at 90 days postwounding, the epidermis of these mice appeared less mature with lower levels of E‐cadherin and cytokeratin 18. The underlying basement membrane, a product of both dermal fibroblasts and epidermal keratinocytes, was not fully established with persistent diffuse expression of the matrix components laminin 5, collagen IV, and collagen VII throughout the wound bed. These results suggest that CXCR3 and its ligands play an important role in the re‐establishment of the basement membrane and epidermis. These studies further establish the emerging signaling network that involves the CXCR3 chemokine receptor and its ligands as a key regulator of wound repair.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Delayed reepithelialization and basement membrane regeneration after wounding in mice lacking CXCR3</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Deficient epithelial repair in CXCR3−/− mice</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Delayed reepithelialization and basement membrane regeneration after wounding in mice lacking CXCR3</title></titleInfo><name type="personal"><namePart type="given">Cecelia C.</namePart><namePart type="family">Yates</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania,</affiliation><affiliation>Pittsburgh VAMC, Pittsburgh, Pennsylvania,</affiliation><affiliation>Tuskegee University Carver Research Foundation, Tuskegee, Alabama, and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Diana</namePart><namePart type="family">Whaley</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Pittsburgh VAMC, Pittsburgh, Pennsylvania,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shveta</namePart><namePart type="family">Hooda</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Patricia A.</namePart><namePart type="family">Hebda</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Richard J.</namePart><namePart type="family">Bodnar</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania,</affiliation><affiliation>Pittsburgh VAMC, Pittsburgh, Pennsylvania,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alan</namePart><namePart type="family">Wells</namePart><namePart type="termsOfAddress">MD, DMSc</namePart><affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania,</affiliation><affiliation>Pittsburgh VAMC, Pittsburgh, Pennsylvania,</affiliation><affiliation>Tuskegee University Carver Research Foundation, Tuskegee, Alabama, and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Inc</publisher><place><placeTerm type="text">Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2009-01</dateIssued><edition>Manuscript received: December 5, 2007Accepted in final form: June 30, 2008</edition><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">4</extent><extent unit="tables">0</extent><extent unit="formulas">0</extent><extent unit="references">20</extent><extent unit="linksCrossRef">57</extent><extent unit="words">5628</extent></physicalDescription><abstract lang="en">Wound healing is a complex, orchestrated series of biological events that is controlled by extracellular components that communicate between cell types to re‐establish lost tissue. We have found that signaling by ELR‐negative CXC chemokines through their common CXCR3 receptor is critical for dermal maturation during the resolving phase. In addition there needs to be complete maturation of the epidermis and regeneration of a delineating basement membrane for proper functioning. The role of this ligand–receptor system appears confounding as one ligand, CXCL4/(PF4), is present during the initial dissolution and two others, CXCL10/(IP‐10) and CXCL11/(IP‐9/I‐TAC), are expressed by keratinocytes in the later regenerative and resolving phases during which the basement membrane is re‐established. We examined CXCR3 signaling role in healing using a mouse lacking this receptor, as all three ligands act solely via the common receptor. Reepithelialization was delayed in CXCR3‐deficient mice in both full and partial‐thickness excisional wounds. Even at 90 days postwounding, the epidermis of these mice appeared less mature with lower levels of E‐cadherin and cytokeratin 18. The underlying basement membrane, a product of both dermal fibroblasts and epidermal keratinocytes, was not fully established with persistent diffuse expression of the matrix components laminin 5, collagen IV, and collagen VII throughout the wound bed. These results suggest that CXCR3 and its ligands play an important role in the re‐establishment of the basement membrane and epidermis. These studies further establish the emerging signaling network that involves the CXCR3 chemokine receptor and its ligands as a key regulator of wound repair.</abstract><relatedItem type="host"><titleInfo><title>Wound Repair and Regeneration</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">1067-1927</identifier><identifier type="eISSN">1524-475X</identifier><identifier type="DOI">10.1111/(ISSN)1524-475X</identifier><identifier type="PublisherID">WRR</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>34</start><end>41</end><total>8</total></extent></part></relatedItem><identifier type="istex">796A25BFC05828B48A6CD9861AD088B3B8B85F79</identifier><identifier type="ark">ark:/67375/WNG-7J87D5Q8-H</identifier><identifier type="DOI">10.1111/j.1524-475X.2008.00439.x</identifier><identifier type="ArticleID">WRR439</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2009 by the Wound Healing Society</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Publishing Inc</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/796A25BFC05828B48A6CD9861AD088B3B8B85F79/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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