Please use this identifier to cite or link to this item:
Title: Regulation of the expression of prostate apoptosis response protein 4 (Par-4) in rat granulosa cells
Authors: González, Inmaculada Hernández 
Santana, Pino 
Gonzalez-Robayna, Ignacio 
Ferrer, Milagros 
Morales, Victoria
López Blanco, Félix 
Fanjul, Luisa F. 
UNESCO Clasification: 32 Ciencias médicas
3205 Medicina interna
Keywords: Protein-Kinase-C
Prostate Apoptosis Response-4
Ventral Prostate
Follicular Atresia
Down-Regulation, et al
Issue Date: 2007
Journal: Apoptosis : an international journal on programmed cell death 
Abstract: The par-4 gene, directs the expression of a protein in the rat ventral prostate after apoptotic stimuli but not growth stimulatory, growth arresting or necrotic signals. Since Par-4 expression appears to be ubiquitous we investigated the possibility of Par-4 having a role in the rat ovary granulosa cells apoptotic death. Par-4 mRNA was detected by RT-PCR with oligonucleotides designed to prime Par-4 leucine zipper in the ovaries of 12 day old rats and reached the higher levels in 24 days old rats. In situ hybridization analysis revealed that Par-4 expression is restricted to granulosa cells. PMSG priming of 24 day old rats for 2 days greatly reduced Par-4 expression in granulosa cells as determined by in situ hybridization, RT-PCR of mRNA and protein immunodetection with Western blot. Granulosa cells placed in serum-fee culture, exhibited increased levels of Par-4 mRNA and protein, in good correlation with the degree of apoptosis. The culture-induced increases in Par-4 are significantly prevented by FSH. Transient transfection of granulosa cells with Par-4 leucine zipper domain that functions as a dominant-negative regulator of Par-4 activity resulted in lower rates of apoptosis while overexpression of the full length Par-4 counteracted FSH effects on apoptosis. Par-4 association with PKC zeta which is supposed to inhibit this kinase mediated antiapoptotic way is also prevented by FSH and, FSH antiapoptotic effects are counteracted by a PKC zeta specific inhibitor. These findings indicate that FSH by suppressing Par-4 expression in the ovary activates PKC zeta-dependent antiapoptotic pathway and suggest that Par-4 is part of the mechanism underlying granulosa cells apoptotic demise.
ISSN: 1360-8185
DOI: 10.1007/s10495-006-0019-7
Source: Apoptosis[ISSN 1360-8185],v. 12 (4), p. 769-779
Appears in Collections:Artículos
Show full item record


checked on Mar 26, 2023


checked on Oct 2, 2022

Page view(s)

checked on Feb 18, 2023

Google ScholarTM




Export metadata

Items in accedaCRIS are protected by copyright, with all rights reserved, unless otherwise indicated.