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Papers In Press, published online ahead of print July 22, 2002
Department of Neurodegeneration, Max Planck Institute of Psychiatry, Munich D-80804
Corresponding Author: chris{at}mpipsykl.mpg.de
Summary Estrogen receptors (ERalpha/ERbeta) are expressed in neuronal cells and exhibit a variety of activities in the central nervous system. ER activity is regulated in a ligand-dependent manner and by co-regulatory factors. Caveolin-1 is a recently identified co-activator of ERalpha mediating the ligand-independent activation of this steroid receptor. Here, the influence of ERs on caveolin expression in human neuroblastoma SK-N-MC cells as well as in rodent brain was investigated. We found that ectopic expression of ERalpha in SK-N-MC cells (SK-ERalpha) leads to a ligand-independent transcriptional suppression of caveolin-1/-2 genes. This suppression is specifically mediated by ERalpha and not ERbeta since ERbeta counteracts the observed caveolin-silencing process.?Interestingly, decreased caveolin expression in SK-ERalpha is accompanied by changes in the methylation pattern of caveolin promoters. The analysis of selected promoter regions of the human caveolin-1 gene showed that certain CpG dinucleotides were hypermethylated in SK-ERalpha cells while the same sites were unmethylated in control, ERbeta- and ERalpha/beta-co-expressing SK-N-MC cells. Inhibition of DNA methylation or histone deacetylation led to partial re-expression of caveolin-1/-2 genes in SK-ERalpha. In vivo-analysis revealed a down-regulation of caveolin-1 expression after long-term estrogen exposure in certain regions of the mouse brain. In conclusion, we have shown for the first time that ERalpha and not ERbeta silences caveolin-1/-2 expression in an epigenetic fashion in neuronal cells. The observed mechanism of gene silencing by ER may have implications for the transcriptional regulation of further ERalpha target genes.
J. Biol. Chem, 10.1074/jbc.M205664200
Submitted on June 7, 2002
Revised on July 22, 2002
Accepted on July 22, 2002
Estrogen receptor alpha-mediated silencing of caveolin gene expression in neuronal cells
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