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Estradiol differentially induces progesterone receptor isoforms expression through alternative promoter regulation in a mouse embryonic hypothalamic cell line

dc.rights.licensehttp://creativecommons.org/licenses/by/4.0es_MX
dc.creatorEDGAR RICARDO VAZQUEZ MARTINEZes_MX
dc.creatorIgnacio Camacho Arroyoes_MX
dc.creatorANGEL ALFONSO ZARAIN HERZBERGes_MX
dc.creatorMARIA DEL CARMEN RODRIGUEZ GUTIERREZes_MX
dc.creatorLUCIANO MENDOZA GARCESes_MX
dc.creatorpatricia ostrosky-wegmanes_MX
dc.creatorMARCO ANTONIO CERBON CERVANTESes_MX
dc.date2016
dc.date.accessioned2021-12-06T22:37:05Z
dc.date.available2021-12-06T22:37:05Z
dc.identifier.urihttp://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17330
dc.descriptionProgesterone receptor (PR) presents two main isoforms (PR-A and PR-B) that are regulated by two specific promoters and transcribed from alternative transcriptional start sites. The molecular regulation of PR isoforms expression in embryonic hypothalamus is poorly understood. The aim of the present study was to assess estradiol regulation of PR isoforms in a mouse embryonic hypothalamic cell line (mHypoE-N42), as well as the transcriptional status of their promoters. MHypoE-N42 cells were treated with estradiol for 6 and 12 h. Then, Western blot, real-time quantitative reverse transcription polymerase chain reaction, and chromatin and DNA immunoprecipitation experiments were performed. PR-B expression was transiently induced by estradiol after 6 h of treatment in an estrogen receptor alpha (ERα)-dependent manner. This induction was associated with an increase in ERα phosphorylation (serine 118) and its recruitment to PR-B promoter. After 12 h of estradiol exposure, a downregulation of this PR isoform was associated with a decrease of specific protein 1, histone 3 lysine 4 trimethylation, and RNA polymerase II occupancy on PR-B promoter, without changes in DNA methylation and hydroxymethylation. In contrast, there were no estradiol-dependent changes in PR-A expression that could be related with the epigenetic marks or the transcription factors evaluated. We demonstrate that PR isoforms are differentially regulated by estradiol and that the induction of PR-B expression is associated to specific transcription factors interactions and epigenetic changes in its promoter in embryonic hypothalamic cells.es_MX
dc.formatAdobe PDFes_MX
dc.languageenges_MX
dc.publisherSpringeres_MX
dc.relationhttps://link.springer.com/article/10.1007/s12020-015-0825-1es_MX
dc.relation.requiresSies_MX
dc.rightsAcceso Abiertoes_MX
dc.sourceEndocrine (1559-0100) Vol. 52 (2016)es_MX
dc.subjectBIOLOGÍA Y QUÍMICAes_MX
dc.subjectBiología moleculares_MX
dc.subjectIsoformas del receptor de progesteronaes_MX
dc.subjectProgesterone receptor isoformses_MX
dc.subjectMarcas epigenéticases_MX
dc.subjectEpigenetic markses_MX
dc.subjectHipotálamoes_MX
dc.subjectHypothalamuses_MX
dc.subjectAcetilación de histonases_MX
dc.subjectHistone acetylationes_MX
dc.subjectEstradioles_MX
dc.titleEstradiol differentially induces progesterone receptor isoforms expression through alternative promoter regulation in a mouse embryonic hypothalamic cell linees_MX
dc.typeArtículoes_MX
dc.audienceResearcherses_MX
dc.creator.idVAME860202HDFZRD04es_MX
dc.creator.idCAAI620909HMCMRG02es_MX
dc.creator.idZAHA560802HDFRRN16es_MX
dc.creator.idROGC620328MCSDTR07es_MX
dc.creator.idMEGL740605HDFNRC04es_MX
dc.creator.idCA1217163es_MX
dc.creator.idCECM520525HDFRRR05es_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercaes_MX
dc.creator.nameIdentifiercurpes_MX


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