Title: Partial silencing of methyl cytosine protein binding 2 ( <i>MECP2</i> ) in mesenchymal stem cells induces senescence with an increase in damaged DNA
Abstract: The FASEB JournalVolume 24, Issue 5 p. 1593-1603 Research CommunicationFree to Read Partial silencing of methyl cytosine protein binding 2 (MECP2) in mesenchymal stem cells induces senescence with an increase in damaged DNA Correction(s) for this article Errata Volume 30Issue 5The FASEB Journal pages: 2064-2064 First Published online: May 1, 2016 Errata Volume 30Issue 5The FASEB Journal pages: 2064-2064 First Published online: May 1, 2016 Tiziana Squillaro, Tiziana Squillaro Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USASearch for more papers by this authorNicola Alessio, Nicola Alessio Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USASearch for more papers by this authorMarilena Cipollaro, Marilena Cipollaro Department of Experimental Medicine, Biotechnology and Molecular Biology Section, Second University of Naples, Naples, ItalySearch for more papers by this authorAlessandra Renieri, Alessandra Renieri Department of Medical Genetics, Philadelphia, Pennsylvania, USASearch for more papers by this authorAntonio Giordano, Antonio Giordano Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USA Department of Human Pathology, Oncology University of Siena, Sienna, Italy Human Health Foundation, Spoleto, ItalySearch for more papers by this authorUmberto Galderisi, Corresponding Author Umberto Galderisi [email protected] Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USACorrespondence: Department of Experimental Medicine, Biotechnology and Molecular Biology Section, Second University of Naples, Via Costantinopoli 16, 80138 Napoli, Italy. E-mail [email protected] for more papers by this author Tiziana Squillaro, Tiziana Squillaro Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USASearch for more papers by this authorNicola Alessio, Nicola Alessio Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USASearch for more papers by this authorMarilena Cipollaro, Marilena Cipollaro Department of Experimental Medicine, Biotechnology and Molecular Biology Section, Second University of Naples, Naples, ItalySearch for more papers by this authorAlessandra Renieri, Alessandra Renieri Department of Medical Genetics, Philadelphia, Pennsylvania, USASearch for more papers by this authorAntonio Giordano, Antonio Giordano Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USA Department of Human Pathology, Oncology University of Siena, Sienna, Italy Human Health Foundation, Spoleto, ItalySearch for more papers by this authorUmberto Galderisi, Corresponding Author Umberto Galderisi [email protected] Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USACorrespondence: Department of Experimental Medicine, Biotechnology and Molecular Biology Section, Second University of Naples, Via Costantinopoli 16, 80138 Napoli, Italy. E-mail [email protected] for more papers by this author First published: 11 January 2010 https://doi.org/10.1096/fj.09-143057Citations: 6Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract DNA methylation is an epigenetic modification that occurs almost exclusively on CpG dinucleotides. MECP2 is a member of a family of proteins that preferentially bind to methylated CpGs. We analyzed the contribution of MECP2 to the physiology of mesenchymal stem cells (MSCs). Partial silencing of MECP2 in human MSCs induced a significant reduction of S-phase cells, along with an increase in G1 cells. These changes were accompanied by a reduction of apoptosis, the triggering of senescence, a decrease in telomerase activity, and the down-regulation of genes involved in maintaining stem cell properties. Senescence appeared to rely on impairment of DNA damage repair and seemed to occur through RB- and P53-related pathways. The effects of MECP2 silencing could be related to the modification of the DNA methylation status. Our results indicate that the silencing of MECP2 induces an increase in methylated cytosines in the genome. Nevertheless, MECP2 partial silencing did not change the methylation of promoters, whose expression is affected by MECP2 down-regulation.—Squillaro, T., Alessio, N., Cipollaro, M., Renieri, A., Giordano, A., Galderisi, U. Partial silencing of methyl cytosine protein binding 2 (MECP2) in mesenchymal stem cells induces senescence with an increase in damaged DNA FASEB J. 24, 1593–1603 (2010). www.fasebj.org Citing Literature Supporting Information Filename Description fsb2fj09143057-sup-0001.zipZip archive, 639.7 KB supplementary material Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. Volume24, Issue5May 2010Pages 1593-1603 RelatedInformation
Publication Year: 2010
Publication Date: 2010-01-11
Language: en
Type: article
Indexed In: ['crossref', 'pubmed']
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Cited By Count: 39
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