Small Cytoskeleton-Associated Molecule, Fibroblast Growth Factor Receptor 1 Oncogene Partner 2/Wound Inducible Transcript-3.0 (FGFR1OP2/wit3.0), Facilitates Fibroblast-Driven Wound Closure
Identifieur interne : 002315 ( Pmc/Checkpoint ); précédent : 002314; suivant : 002316Small Cytoskeleton-Associated Molecule, Fibroblast Growth Factor Receptor 1 Oncogene Partner 2/Wound Inducible Transcript-3.0 (FGFR1OP2/wit3.0), Facilitates Fibroblast-Driven Wound Closure
Auteurs : Audrey Lin [États-Unis] ; Akishige Hokugo [États-Unis] ; Jae Choi [États-Unis] ; Ichiro Nishimura [États-Unis]Source :
- The American Journal of Pathology [ 0002-9440 ] ; 2010.
Abstract
Wounds created in the oral cavity heal rapidly and leave minimal scarring. We have examined a role of a previously isolated cDNA from oral wounds encoding wound inducible transcript-3.0 (wit3.0), also known as fibroblast growth factor receptor 1 oncogene partner 2 (FGFR1OP2). FGFR1OP2/wit3.0 was highly expressed in oral wound fibroblasts without noticeable up-regulation of α-smooth muscle actin. In silico analyses, denaturing and nondenaturing gel Western blot, and immunocytology together demonstrated that FGFR1OP2/wit3.0 were able to dimerize and oligomerize through coiled-coil structures and appeared to associate with cytoskeleton networks in oral wound fibroblasts. Overexpression of FGFR1OP2/wit3.0 increased the floating collagen gel contraction of naïve oral fibroblasts to the level of oral wound fibroblasts, which was in turn attenuated by small-interfering RNA knockdown. The FGFR1OP2/wit3.0 synthesis did not affect the expression of collagen I as well as procontractile peptides such as α-smooth muscle actin, and transforming growth factor-β1 had no effect on FGFR1OP2/wit3.0 expression. Fibroblastic cells derived from embryonic stem cells carrying FGFR1OP2/wit3.0 (+/−) mutation showed significant retardation in cell migration. Thus, we postulate that FGFR1OP2/wit3.0 may regulate cell motility and stimulate wound closure. FGFR1OP2/wit3.0 was not up-regulated during skin wound healing; however, when treated with FGFR1OP2/wit3.0 -expression vector, the skin wound closure was significantly accelerated, resulting in the limited granulation tissue formation. Our data suggest that FGFR1OP2/wit3.0 may possess a therapeutic potential for wound management.
Url:
DOI: 10.2353/ajpath.2010.090256
PubMed: 19959814
PubMed Central: 2797874
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Small Cytoskeleton-Associated Molecule, Fibroblast Growth Factor Receptor 1 Oncogene Partner 2/Wound Inducible Transcript-3.0 (FGFR1OP2/wit3.0), Facilitates Fibroblast-Driven Wound Closure</title><author><name sortKey="Lin, Audrey" sort="Lin, Audrey" uniqKey="Lin A" first="Audrey" last="Lin">Audrey Lin</name><affiliation wicri:level="2"><nlm:aff id="aff1">Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="aff2">Division of Advanced Prosthodontics, Biomaterials and Hospital Dentistry, School of Dentistry, the Biomedical Engineering Interdepartmental Program, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Division of Advanced Prosthodontics, Biomaterials and Hospital Dentistry, School of Dentistry, the Biomedical Engineering Interdepartmental Program, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Hokugo, Akishige" sort="Hokugo, Akishige" uniqKey="Hokugo A" first="Akishige" last="Hokugo">Akishige Hokugo</name><affiliation wicri:level="2"><nlm:aff id="aff1">Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Choi, Jae" sort="Choi, Jae" uniqKey="Choi J" first="Jae" last="Choi">Jae Choi</name><affiliation wicri:level="2"><nlm:aff id="aff1">Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="aff3">Henry Samueli School of Engineering and Applied Science, and the Section of Periodontics, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Henry Samueli School of Engineering and Applied Science, and the Section of Periodontics, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Nishimura, Ichiro" sort="Nishimura, Ichiro" uniqKey="Nishimura I" first="Ichiro" last="Nishimura">Ichiro Nishimura</name><affiliation wicri:level="2"><nlm:aff id="aff1">Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">19959814</idno><idno type="pmc">2797874</idno><idno 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Lin</name><affiliation wicri:level="2"><nlm:aff id="aff1">Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="aff2">Division of Advanced Prosthodontics, Biomaterials and Hospital Dentistry, School of Dentistry, the Biomedical Engineering Interdepartmental Program, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Division of Advanced Prosthodontics, Biomaterials and Hospital Dentistry, School of Dentistry, the Biomedical Engineering Interdepartmental Program, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Hokugo, Akishige" sort="Hokugo, Akishige" uniqKey="Hokugo A" first="Akishige" last="Hokugo">Akishige Hokugo</name><affiliation wicri:level="2"><nlm:aff id="aff1">Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Choi, Jae" sort="Choi, Jae" uniqKey="Choi J" first="Jae" last="Choi">Jae Choi</name><affiliation wicri:level="2"><nlm:aff id="aff1">Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="aff3">Henry Samueli School of Engineering and Applied Science, and the Section of Periodontics, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Henry Samueli School of Engineering and Applied Science, and the Section of Periodontics, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation></author><author><name sortKey="Nishimura, Ichiro" sort="Nishimura, Ichiro" uniqKey="Nishimura I" first="Ichiro" last="Nishimura">Ichiro Nishimura</name><affiliation wicri:level="2"><nlm:aff id="aff1">Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles, California</nlm:aff><country>États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles</wicri:cityArea></affiliation></author></analytic><series><title level="j">The American Journal of Pathology</title><idno type="ISSN">0002-9440</idno><idno type="eISSN">1525-2191</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Wounds created in the oral cavity heal rapidly and leave minimal scarring. We have examined a role of a previously isolated cDNA from oral wounds encoding wound inducible transcript-3.0 (wit3.0), also known as fibroblast growth factor receptor 1 oncogene partner 2 (FGFR1OP2). FGFR1OP2/wit3.0 was highly expressed in oral wound fibroblasts without noticeable up-regulation of α-smooth muscle actin. In silico analyses, denaturing and nondenaturing gel Western blot, and immunocytology together demonstrated that FGFR1OP2/wit3.0 were able to dimerize and oligomerize through coiled-coil structures and appeared to associate with cytoskeleton networks in oral wound fibroblasts. Overexpression of FGFR1OP2/wit3.0 increased the floating collagen gel contraction of naïve oral fibroblasts to the level of oral wound fibroblasts, which was in turn attenuated by small-interfering RNA knockdown. The FGFR1OP2/wit3.0 synthesis did not affect the expression of collagen I as well as procontractile peptides such as α-smooth muscle actin, and transforming growth factor-β1 had no effect on FGFR1OP2/wit3.0 expression. Fibroblastic cells derived from embryonic stem cells carrying FGFR1OP2/wit3.0 (+/−) mutation showed significant retardation in cell migration. Thus, we postulate that FGFR1OP2/wit3.0 may regulate cell motility and stimulate wound closure. FGFR1OP2/wit3.0 was not up-regulated during skin wound healing; however, when treated with FGFR1OP2/wit3.0 -expression vector, the skin wound closure was significantly accelerated, resulting in the limited granulation tissue formation. Our data suggest that FGFR1OP2/wit3.0 may possess a therapeutic potential for wound management.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Pathol</journal-id><journal-title-group><journal-title>The American Journal of Pathology</journal-title></journal-title-group><issn pub-type="ppub">0002-9440</issn><issn pub-type="epub">1525-2191</issn><publisher><publisher-name>American Society for Investigative Pathology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">19959814</article-id><article-id pub-id-type="pmc">2797874</article-id><article-id pub-id-type="publisher-id">AJPA60329</article-id><article-id pub-id-type="doi">10.2353/ajpath.2010.090256</article-id><article-categories><subj-group subj-group-type="heading"><subject>Regular Articles</subject></subj-group></article-categories><title-group><article-title>Small Cytoskeleton-Associated Molecule, Fibroblast Growth Factor Receptor 1 Oncogene Partner 2/Wound Inducible Transcript-3.0 (FGFR1OP2/wit3.0), Facilitates Fibroblast-Driven Wound Closure</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lin</surname><given-names>Audrey</given-names></name><xref rid="aff1" ref-type="aff">*</xref><xref rid="aff2" ref-type="aff">†</xref></contrib><contrib contrib-type="author"><name><surname>Hokugo</surname><given-names>Akishige</given-names></name><xref rid="aff1" ref-type="aff">*</xref></contrib><contrib contrib-type="author"><name><surname>Choi</surname><given-names>Jae</given-names></name><xref rid="aff1" ref-type="aff">*</xref><xref rid="aff3" ref-type="aff">‡</xref></contrib><contrib contrib-type="author"><name><surname>Nishimura</surname><given-names>Ichiro</given-names></name><email>inishimura@dentistry.ucla.edu</email><xref rid="aff1" ref-type="aff">*</xref><xref rid="cor1" ref-type="corresp">*</xref></contrib></contrib-group><aff id="aff1"><label>*</label>Weintraub Center for Reconstructive Biotechnology, School of Dentistry, University of California, Los Angeles, Los Angeles, California</aff><aff id="aff2"><label>†</label>Division of Advanced Prosthodontics, Biomaterials and Hospital Dentistry, School of Dentistry, the Biomedical Engineering Interdepartmental Program, School of Dentistry, University of California, Los Angeles, Los Angeles, California</aff><aff id="aff3"><label>‡</label>Henry Samueli School of Engineering and Applied Science, and the Section of Periodontics, School of Dentistry, University of California, Los Angeles, Los Angeles, California</aff><author-notes><corresp id="cor1"><label>*</label>Address reprint requests to Ichiro Nishimura, The Weintraub Center for Reconstructive Biotechnology, University of California, Los Angeles, School of Dentistry, Box 951668, CHS B3-087, Los Angeles, CA 90095-1668 <email>inishimura@dentistry.ucla.edu</email></corresp></author-notes><pub-date pub-type="ppub"><month>1</month><year>2010</year></pub-date><volume>176</volume><issue>1</issue><fpage>108</fpage><lpage>121</lpage><history><date date-type="accepted"><day>15</day><month>9</month><year>2009</year></date></history><permissions><copyright-statement>© 2010 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2010</copyright-year><copyright-holder>American Society for Investigative Pathology</copyright-holder></permissions><abstract><p>Wounds created in the oral cavity heal rapidly and leave minimal scarring. We have examined a role of a previously isolated cDNA from oral wounds encoding wound inducible transcript-3.0 (wit3.0), also known as fibroblast growth factor receptor 1 oncogene partner 2 (FGFR1OP2). FGFR1OP2/wit3.0 was highly expressed in oral wound fibroblasts without noticeable up-regulation of α-smooth muscle actin. In silico analyses, denaturing and nondenaturing gel Western blot, and immunocytology together demonstrated that FGFR1OP2/wit3.0 were able to dimerize and oligomerize through coiled-coil structures and appeared to associate with cytoskeleton networks in oral wound fibroblasts. Overexpression of FGFR1OP2/wit3.0 increased the floating collagen gel contraction of naïve oral fibroblasts to the level of oral wound fibroblasts, which was in turn attenuated by small-interfering RNA knockdown. The FGFR1OP2/wit3.0 synthesis did not affect the expression of collagen I as well as procontractile peptides such as α-smooth muscle actin, and transforming growth factor-β1 had no effect on FGFR1OP2/wit3.0 expression. Fibroblastic cells derived from embryonic stem cells carrying FGFR1OP2/wit3.0 (+/−) mutation showed significant retardation in cell migration. Thus, we postulate that FGFR1OP2/wit3.0 may regulate cell motility and stimulate wound closure. FGFR1OP2/wit3.0 was not up-regulated during skin wound healing; however, when treated with FGFR1OP2/wit3.0 -expression vector, the skin wound closure was significantly accelerated, resulting in the limited granulation tissue formation. Our data suggest that FGFR1OP2/wit3.0 may possess a therapeutic potential for wound management.</p></abstract></article-meta></front></pmc><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Lin, Audrey" sort="Lin, Audrey" uniqKey="Lin A" first="Audrey" last="Lin">Audrey Lin</name></region><name sortKey="Choi, Jae" sort="Choi, Jae" uniqKey="Choi J" first="Jae" last="Choi">Jae Choi</name><name sortKey="Choi, Jae" sort="Choi, Jae" uniqKey="Choi J" first="Jae" last="Choi">Jae Choi</name><name sortKey="Hokugo, Akishige" sort="Hokugo, Akishige" uniqKey="Hokugo A" first="Akishige" last="Hokugo">Akishige Hokugo</name><name sortKey="Lin, Audrey" sort="Lin, Audrey" uniqKey="Lin A" first="Audrey" last="Lin">Audrey Lin</name><name sortKey="Nishimura, Ichiro" sort="Nishimura, Ichiro" uniqKey="Nishimura I" first="Ichiro" last="Nishimura">Ichiro Nishimura</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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