ANKRD1 Acts as a Transcriptional Repressor of MMP13 via the AP-1 Site
Identifieur interne : 003089 ( Pmc/Corpus ); précédent : 003088; suivant : 003090ANKRD1 Acts as a Transcriptional Repressor of MMP13 via the AP-1 Site
Auteurs : Karinna Almod Var-García ; Minjae Kwon ; Susan E. Samaras ; Jeffrey M. DavidsonSource :
- Molecular and Cellular Biology [ 0270-7306 ] ; 2014.
Abstract
The transcriptional cofactor ANKRD1 is sharply induced during wound repair, and its overexpression enhances healing. We recently found that global deletion of murine
Url:
DOI: 10.1128/MCB.01357-13
PubMed: 24515436
PubMed Central: 3993579
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PMC:3993579Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">ANKRD1 Acts as a Transcriptional Repressor of <italic>MMP13</italic>
via the AP-1 Site</title>
<author><name sortKey="Almod Var Garcia, Karinna" sort="Almod Var Garcia, Karinna" uniqKey="Almod Var Garcia K" first="Karinna" last="Almod Var-García">Karinna Almod Var-García</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Kwon, Minjae" sort="Kwon, Minjae" uniqKey="Kwon M" first="Minjae" last="Kwon">Minjae Kwon</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Samaras, Susan E" sort="Samaras, Susan E" uniqKey="Samaras S" first="Susan E." last="Samaras">Susan E. Samaras</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Davidson, Jeffrey M" sort="Davidson, Jeffrey M" uniqKey="Davidson J" first="Jeffrey M." last="Davidson">Jeffrey M. Davidson</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="aff2">VA Tennessee Valley Healthcare System, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
</author>
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<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993579</idno>
<idno type="RBID">PMC:3993579</idno>
<idno type="doi">10.1128/MCB.01357-13</idno>
<date when="2014">2014</date>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">ANKRD1 Acts as a Transcriptional Repressor of <italic>MMP13</italic>
via the AP-1 Site</title>
<author><name sortKey="Almod Var Garcia, Karinna" sort="Almod Var Garcia, Karinna" uniqKey="Almod Var Garcia K" first="Karinna" last="Almod Var-García">Karinna Almod Var-García</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Kwon, Minjae" sort="Kwon, Minjae" uniqKey="Kwon M" first="Minjae" last="Kwon">Minjae Kwon</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Samaras, Susan E" sort="Samaras, Susan E" uniqKey="Samaras S" first="Susan E." last="Samaras">Susan E. Samaras</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Davidson, Jeffrey M" sort="Davidson, Jeffrey M" uniqKey="Davidson J" first="Jeffrey M." last="Davidson">Jeffrey M. Davidson</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="aff2">VA Tennessee Valley Healthcare System, Nashville, Tennessee, USA</nlm:aff>
</affiliation>
</author>
</analytic>
<series><title level="j">Molecular and Cellular Biology</title>
<idno type="ISSN">0270-7306</idno>
<idno type="eISSN">1098-5549</idno>
<imprint><date when="2014">2014</date>
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<front><div type="abstract" xml:lang="en"><p>The transcriptional cofactor ANKRD1 is sharply induced during wound repair, and its overexpression enhances healing. We recently found that global deletion of murine <italic>Ankrd1</italic>
impairs wound contraction and enhances necrosis of ischemic wounds. A quantitative PCR array of <italic>Ankrd1</italic>
<sup>−/−</sup>
(KO) fibroblasts indicated that ANKRD1 regulates MMP genes. Yeast two-hybrid and coimmunoprecipitation analyses associated ANKRD1 with nucleolin, which represses AP-1 activation of <italic>MMP13. Ankrd1</italic>
deletion enhanced both basal and phorbol 12-myristate 13-acetate (PMA)-induced <italic>MMP13</italic>
promoter activity; conversely, <italic>Ankrd1</italic>
overexpression in control cells decreased PMA-induced <italic>MMP13</italic>
promoter activity. <italic>Ankrd1</italic>
reconstitution in KO fibroblasts decreased <italic>MMP13</italic>
mRNA, while <italic>Ankrd1</italic>
knockdown increased these levels. <italic>MMP13</italic>
mRNA and protein were elevated in intact skin and wounds of KO versus <italic>Ankrd1</italic>
<sup><italic>fl/fl</italic>
</sup>
(FLOX) mice. Electrophoretic mobility shift assay gel shift patterns suggested that additional transcription factors bind to the <italic>MMP13</italic>
AP-1 site in the absence of <italic>Ankrd1</italic>
, and this concept was reinforced by chromatin immunoprecipitation analysis as greater binding of c-Jun to the AP-1 site in extracts from FLOX versus KO fibroblasts. We propose that ANKRD1, in association with factors such as nucleolin, represses <italic>MMP13</italic>
transcription. <italic>Ankrd1</italic>
deletion additionally relieved <italic>MMP10</italic>
transcriptional repression. Nuclear ANKRD1 appears to modulate extracellular matrix remodeling by MMPs.</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">Mol Cell Biol</journal-id>
<journal-id journal-id-type="iso-abbrev">Mol. Cell. Biol</journal-id>
<journal-id journal-id-type="hwp">mcb</journal-id>
<journal-id journal-id-type="pmc">mcb</journal-id>
<journal-id journal-id-type="publisher-id">MCB</journal-id>
<journal-title-group><journal-title>Molecular and Cellular Biology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0270-7306</issn>
<issn pub-type="epub">1098-5549</issn>
<publisher><publisher-name>American Society for Microbiology</publisher-name>
<publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">24515436</article-id>
<article-id pub-id-type="pmc">3993579</article-id>
<article-id pub-id-type="publisher-id">01357-13</article-id>
<article-id pub-id-type="doi">10.1128/MCB.01357-13</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Articles</subject>
</subj-group>
</article-categories>
<title-group><article-title>ANKRD1 Acts as a Transcriptional Repressor of <italic>MMP13</italic>
via the AP-1 Site</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Almodóvar-García</surname>
<given-names>Karinna</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kwon</surname>
<given-names>Minjae</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Samaras</surname>
<given-names>Susan E.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Davidson</surname>
<given-names>Jeffrey M.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>b</sup>
</xref>
</contrib>
<aff id="aff1"><label>a</label>
Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA</aff>
<aff id="aff2"><label>b</label>
VA Tennessee Valley Healthcare System, Nashville, Tennessee, USA</aff>
</contrib-group>
<author-notes><corresp id="cor1">Address correspondence to Jeffrey M. Davidson, <email>jeff.davidson@vanderbilt.edu</email>
.</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>4</month>
<year>2014</year>
</pub-date>
<volume>34</volume>
<issue>8</issue>
<fpage>1500</fpage>
<lpage>1511</lpage>
<history><date date-type="received"><day>9</day>
<month>10</month>
<year>2013</year>
</date>
<date date-type="rev-request"><day>2</day>
<month>12</month>
<year>2013</year>
</date>
<date date-type="accepted"><day>31</day>
<month>1</month>
<year>2014</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2014, American Society for Microbiology. All Rights Reserved.</copyright-statement>
<copyright-year>2014</copyright-year>
<copyright-holder>American Society for Microbiology</copyright-holder>
</permissions>
<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zmb00814001500.pdf"></self-uri>
<abstract><p>The transcriptional cofactor ANKRD1 is sharply induced during wound repair, and its overexpression enhances healing. We recently found that global deletion of murine <italic>Ankrd1</italic>
impairs wound contraction and enhances necrosis of ischemic wounds. A quantitative PCR array of <italic>Ankrd1</italic>
<sup>−/−</sup>
(KO) fibroblasts indicated that ANKRD1 regulates MMP genes. Yeast two-hybrid and coimmunoprecipitation analyses associated ANKRD1 with nucleolin, which represses AP-1 activation of <italic>MMP13. Ankrd1</italic>
deletion enhanced both basal and phorbol 12-myristate 13-acetate (PMA)-induced <italic>MMP13</italic>
promoter activity; conversely, <italic>Ankrd1</italic>
overexpression in control cells decreased PMA-induced <italic>MMP13</italic>
promoter activity. <italic>Ankrd1</italic>
reconstitution in KO fibroblasts decreased <italic>MMP13</italic>
mRNA, while <italic>Ankrd1</italic>
knockdown increased these levels. <italic>MMP13</italic>
mRNA and protein were elevated in intact skin and wounds of KO versus <italic>Ankrd1</italic>
<sup><italic>fl/fl</italic>
</sup>
(FLOX) mice. Electrophoretic mobility shift assay gel shift patterns suggested that additional transcription factors bind to the <italic>MMP13</italic>
AP-1 site in the absence of <italic>Ankrd1</italic>
, and this concept was reinforced by chromatin immunoprecipitation analysis as greater binding of c-Jun to the AP-1 site in extracts from FLOX versus KO fibroblasts. We propose that ANKRD1, in association with factors such as nucleolin, represses <italic>MMP13</italic>
transcription. <italic>Ankrd1</italic>
deletion additionally relieved <italic>MMP10</italic>
transcriptional repression. Nuclear ANKRD1 appears to modulate extracellular matrix remodeling by MMPs.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
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