Secretaría de Gobernación
CONACYT
INGER
Please use this identifier to cite or link to this item: http://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17330
Title: Estradiol differentially induces progesterone receptor isoforms expression through alternative promoter regulation in a mouse embryonic hypothalamic cell line
metadata.dc.creator: EDGAR RICARDO VAZQUEZ MARTINEZ
Ignacio Camacho Arroyo
ANGEL ALFONSO ZARAIN HERZBERG
MARIA DEL CARMEN RODRIGUEZ GUTIERREZ
LUCIANO MENDOZA GARCES
patricia ostrosky-wegman
MARCO ANTONIO CERBON CERVANTES
Keywords: BIOLOGÍA Y QUÍMICA;Biología molecular;Isoformas del receptor de progesterona;Progesterone receptor isoforms;Marcas epigenéticas;Epigenetic marks;Hipotálamo;Hypothalamus;Acetilación de histonas;Histone acetylation;Estradiol
metadata.dc.date: 2016
Publisher: Springer
Description: Progesterone 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.
URI: http://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17330
Appears in Collections:1. Artículos

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