ANKRD1 Acts as a Transcriptional Repressor of MMP13 via the AP-1 Site
Identifieur interne : 002E06 ( Main/Merge ); précédent : 002E05; suivant : 002E07ANKRD1 Acts as a Transcriptional Repressor of MMP13 via the AP-1 Site
Auteurs : Karinna Almod Var-García [États-Unis] ; Minjae Kwon [États-Unis] ; Susan E. Samaras [États-Unis] ; Jeffrey M. Davidson [États-Unis]Source :
- 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
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<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>
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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>
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