Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/328143
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampVeronezi, Giovana Maria Bredapt_BR
dc.contributor.authorunicampFelisbino, Marina Barretopt_BR
dc.contributor.authorunicampGatti, Maria Silvia Viccaript_BR
dc.contributor.authorunicampVidal, Benedicto de Campospt_BR
dc.contributor.authorunicampMello, Maria Luiza Silveirapt_BR
dc.typeOutros documentospt_BR
dc.titleEffects Of Epigenetic Modulator Drugs On Dna Methylation Of Hela Cellsen
dc.titleEffects of epigenetic modulator drugs on DNA methylation of HeLa cellspt_BR
dc.contributor.authorVeronezi, Giovana Maria Bredapt_BR
dc.contributor.authorFelisbino, Marina Barretopt_BR
dc.contributor.authorGatti, Maria Silvia Viccaript_BR
dc.contributor.authorVidal, Benedicto de Campospt_BR
dc.contributor.authorMello, Maria Luiza Silveirapt_BR
dc.subjectCélulas HeLapt_BR
dc.subjectÁcido valproicopt_BR
dc.subjectEpigenéticapt_BR
dc.subjectMetilação de DNApt_BR
dc.subjectCromatinapt_BR
dc.subjectReação em cadeia da polimerasept_BR
dc.subject.otherlanguageHeLa cellspt_BR
dc.subject.otherlanguageValproic acidpt_BR
dc.subject.otherlanguageEpigeneticspt_BR
dc.subject.otherlanguageDNA methylationpt_BR
dc.subject.otherlanguageChromatinpt_BR
dc.subject.otherlanguagePolymerase chain reactionpt_BR
dc.description.abstractValproic acid (VPA) is an important epigenetic drug that works as a histone deacetylase (HDAC) inhibitor, inducing histone hyperacetylation and chromatin unpackaging in several cell types. Currently, DNA demethylation is also being considered part of the VPA action, as shown in HEK293 cells and rat brain cells. This process may occur in a replication-independent active way, possibly with TET proteins participation and 5-hydroxymethylcytosine (5hmC) formation. Recent studies have also detected a 5hmC increase in different cell types after treatment with the well-established DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR), which is known to promote DNA demethylation in a cell cycle-dependent passive way. In the present work, the process of DNA demethylation following VPA and 5-aza-CdR treatment was studied in HeLa cells. The cells were treated with 1.0 m M VPA for 4 h and then cultivated in the absence of the drug for 24 and 48 h or treated with 5.0 ? M 5-Aza-CdR for 28 h. Immunoassays for 5-methylcytosine (5mC) and 5hmC were performed to evaluate changes in signals related to total DNA methylation and hydroxymethylation. Quantitative PCR assays were used to investigate gene expression levels of TET1 and DNMT1 . Lower fluorescence intensity for methylated DNA in contrast to higher fluorescence intensity for hydroxymethylated DNA was observed in VPAand 5-aza-CdR-treated cells compared to untreated controls, which could be related to an active demethylation induction by both drugs. The DNMT1 mRNA levels were not affected by VPA or 5-aza-CdR treatment. TET1 gene expression decreased after VPA exposure, indicating that other enzymes associated with active demethylation may be involved in this process. Interestingly, 5-azaCdR treatment increased TET1 expression, suggesting that the agents analyzed here may promote active demethylation by different pathways. Taken together, these results help to elucidate the multiple effects performed by these drugs on epigenetic markers.pt
dc.description.abstractValproic acid (VPA) is an important epigenetic drug that works as a histone deacetylase (HDAC) inhibitor, inducing histone hyperacetylation and chromatin unpackaging in several cell types. Currently, DNA demethylation is also being considered part of the VPA action, as shown in HEK293 cells and rat brain cells. This process may occur in a replication-independent active way, possibly with TET proteins participation and 5-hydroxymethylcytosine (5hmC) formation. Recent studies have also detected a 5hmC increase in different cell types after treatment with the well-established DNA methyltransferase (DNMT) inhibitor 5-aza-2′-deoxycytidine (5-aza-CdR), which is known to promote DNA demethylation in a cell cycle-dependent passive way. In the present work, the process of DNA demethylation following VPA and 5-aza-CdR treatment was studied in HeLa cells. The cells were treated with 1.0 m M VPA for 4 h and then cultivated in the absence of the drug for 24 and 48 h or treated with 5.0 μ M 5-Aza-CdR for 28 h. Immunoassays for 5-methylcytosine (5mC) and 5hmC were performed to evaluate changes in signals related to total DNA methylation and hydroxymethylation. Quantitative PCR assays were used to investigate gene expression levels of TET1 and DNMT1 . Lower fluorescence intensity for methylated DNA in contrast to higher fluorescence intensity for hydroxymethylated DNA was observed in VPAand 5-aza-CdR-treated cells compared to untreated controls, which could be related to an active demethylation induction by both drugs. The DNMT1 mRNA levels were not affected by VPA or 5-aza-CdR treatment. TET1 gene expression decreased after VPA exposure, indicating that other enzymes associated with active demethylation may be involved in this process. Interestingly, 5-azaCdR treatment increased TET1 expression, suggesting that the agents analyzed here may promote active demethylation by different pathways. Taken together, these results help to elucidate the multiple effects performed by these drugs on epigenetic markers.pt_BR
dc.description.event21. International Chromosome Conferencept_BR
dc.relation.ispartofCytogenetic and genome researchpt_BR
dc.relation.ispartofabbreviationCytogenet. genome res.pt_BR
dc.publisher.cityBaselpt_BR
dc.publisher.countrySuíçapt_BR
dc.publisherKargerpt_BR
dc.date.issued2016pt_BR
dc.date.monthofcirculationJun.pt_BR
dc.identifier.citationCytogenetic And Genome Research. Karger, v. 148, p. 140 - 140, 2016.pt_BR
dc.language.isoengpt_BR
dc.description.volume148pt_BR
dc.description.issuenumber2-3pt_BR
dc.description.firstpage140pt_BR
dc.description.lastpage140pt_BR
dc.rightsfechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn1424-8581pt_BR
dc.identifier.eissn1424-859Xpt_BR
dc.identifier.doi10.1159/000446523pt_BR
dc.identifier.urlhttps://www.karger.com/Article/Abstract/446523pt_BR
dc.description.sponsorshipFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsorship1FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsordocumentnumber2014/23842–0pt_BR
dc.date.available2017-11-13T13:23:38Z-
dc.date.accessioned2017-11-13T13:23:38Z-
dc.description.provenanceMade available in DSpace on 2017-11-13T13:23:38Z (GMT). No. of bitstreams: 1 000378777400136.pdf: 523346 bytes, checksum: 60b73e45d92c39eab6f1f1acbcacac7d (MD5) Previous issue date: 2016en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/328143-
dc.description.conferencenome21. International Chromosome Conferencept_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Genética, Evolução e Bioagentespt_BR
dc.contributor.departmentDepartamento de Biologia Estrutural e Funcionalpt_BR
dc.contributor.departmentDepartamento de Biologia Estrutural e Funcionalpt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.identifier.source000378777400136pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0003-3614-5503pt_BR
dc.creator.orcid0000-0003-0285-1653pt_BR
dc.creator.orcid0000-0003-1629-5619pt_BR
dc.type.formResumo simplespt_BR
dc.type.formResumo simplespt_BR
dc.description.eventsponsorS. Kargerpt_BR
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