SIRT1 activation mediates heat-induced survival of UVB damaged Keratinocytes.
Identifieur interne : 000A27 ( PubMed/Corpus ); précédent : 000A26; suivant : 000A28SIRT1 activation mediates heat-induced survival of UVB damaged Keratinocytes.
Auteurs : Leslie Calapre ; Elin S. Gray ; Sandrine Kurdykowski ; Anthony David ; Pascal Descargues ; Mel ZimanSource :
- BMC dermatology [ 1471-5945 ] ; 2017.
Abstract
Exposure to heat stress after UVB irradiation induces a reduction of apoptosis, resulting in survival of DNA damaged human keratinocytes. This heat-mediated evasion of apoptosis appears to be mediated by activation of SIRT1 and inactivation of p53 signalling. In this study, we assessed the role of SIRT1 in the inactivation of p53 signalling and impairment of DNA damage response in UVB plus heat exposed keratinocytes.
DOI: 10.1186/s12895-017-0060-y
PubMed: 28601088
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pubmed:28601088Le document en format XML
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<author><name sortKey="Descargues, Pascal" sort="Descargues, Pascal" uniqKey="Descargues P" first="Pascal" last="Descargues">Pascal Descargues</name>
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<author><name sortKey="David, Anthony" sort="David, Anthony" uniqKey="David A" first="Anthony" last="David">Anthony David</name>
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<author><name sortKey="Descargues, Pascal" sort="Descargues, Pascal" uniqKey="Descargues P" first="Pascal" last="Descargues">Pascal Descargues</name>
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<series><title level="j">BMC dermatology</title>
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<front><div type="abstract" xml:lang="en">Exposure to heat stress after UVB irradiation induces a reduction of apoptosis, resulting in survival of DNA damaged human keratinocytes. This heat-mediated evasion of apoptosis appears to be mediated by activation of SIRT1 and inactivation of p53 signalling. In this study, we assessed the role of SIRT1 in the inactivation of p53 signalling and impairment of DNA damage response in UVB plus heat exposed keratinocytes.</div>
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<DateCreated><Year>2017</Year>
<Month>06</Month>
<Day>11</Day>
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<DateRevised><Year>2017</Year>
<Month>06</Month>
<Day>15</Day>
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<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-5945</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>17</Volume>
<Issue>1</Issue>
<PubDate><Year>2017</Year>
<Month>Jun</Month>
<Day>10</Day>
</PubDate>
</JournalIssue>
<Title>BMC dermatology</Title>
<ISOAbbreviation>BMC Dermatol.</ISOAbbreviation>
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<ArticleTitle>SIRT1 activation mediates heat-induced survival of UVB damaged Keratinocytes.</ArticleTitle>
<Pagination><MedlinePgn>8</MedlinePgn>
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<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Exposure to heat stress after UVB irradiation induces a reduction of apoptosis, resulting in survival of DNA damaged human keratinocytes. This heat-mediated evasion of apoptosis appears to be mediated by activation of SIRT1 and inactivation of p53 signalling. In this study, we assessed the role of SIRT1 in the inactivation of p53 signalling and impairment of DNA damage response in UVB plus heat exposed keratinocytes.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Activation of SIRT1 after multiple UVB plus heat exposures resulted in increased p53 deacetylation at K382, which is known to affect its binding to specific target genes. Accordingly, we noted decreased apoptosis and down regulation of the p53 targeted pro-apoptotic gene BAX and the DNA repair genes ERCC1 and XPC after UVB plus heat treatments. In addition, UVB plus heat induced increased expression of the cell survival gene Survivin and the proliferation marker Ki67. Notably, keratinocytes exposed to UVB plus heat in the presence of the SIRT1 inhibitor, Ex-527, showed a similar phenotype to those exposed to UV alone; i.e. an increase in p53 acetylation, increased apoptosis and low levels of Survivin.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">This study demonstrate that heat-induced SIRT1 activation mediates survival of DNA damaged keratinocytes through deacetylation of p53 after exposure to UVB plus heat.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Calapre</LastName>
<ForeName>Leslie</ForeName>
<Initials>L</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0001-7595-6523</Identifier>
<AffiliationInfo><Affiliation>School of Medical Science, Edith Cowan University, 270 Joondalup Drive, Joondalup, Perth, WA, 6027, Australia.</Affiliation>
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<Author ValidYN="Y"><LastName>Gray</LastName>
<ForeName>Elin S</ForeName>
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<AffiliationInfo><Affiliation>School of Medical Science, Edith Cowan University, 270 Joondalup Drive, Joondalup, Perth, WA, 6027, Australia.</Affiliation>
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<Author ValidYN="Y"><LastName>Kurdykowski</LastName>
<ForeName>Sandrine</ForeName>
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<Author ValidYN="Y"><LastName>Descargues</LastName>
<ForeName>Pascal</ForeName>
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<AffiliationInfo><Affiliation>GENOSKIN Centre Pierre Potier, Oncopole, Toulouse, France.</Affiliation>
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<Author ValidYN="Y"><LastName>Ziman</LastName>
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<AffiliationInfo><Affiliation>School of Medical Science, Edith Cowan University, 270 Joondalup Drive, Joondalup, Perth, WA, 6027, Australia. m.ziman@ecu.edu.au.</Affiliation>
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<AffiliationInfo><Affiliation>School of Pathology and Laboratory Medicine, University of Western Australia, Crawley, WA, Australia. m.ziman@ecu.edu.au.</Affiliation>
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<Language>eng</Language>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Apoptosis</Keyword>
<Keyword MajorTopicYN="N">Heat stress</Keyword>
<Keyword MajorTopicYN="N">Keratinocytes</Keyword>
<Keyword MajorTopicYN="N">SIRT1</Keyword>
<Keyword MajorTopicYN="N">UVB</Keyword>
<Keyword MajorTopicYN="N">p53</Keyword>
<Keyword MajorTopicYN="N">p53 deacetylation</Keyword>
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