Expression and activity of vitamin D receptor in the human placenta and in choriocarcinoma BeWo and JEG-3 cell lines
Language English Country Ireland Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
19133314
DOI
10.1016/j.mce.2008.12.003
PII: S0303-7207(08)00580-7
Knihovny.cz E-resources
- MeSH
- Transcriptional Activation drug effects MeSH
- Cell Differentiation drug effects MeSH
- Choriocarcinoma genetics metabolism MeSH
- Epigenesis, Genetic drug effects MeSH
- Estradiol pharmacology MeSH
- Genome, Human genetics MeSH
- Cadherins genetics metabolism MeSH
- Calcitriol pharmacology MeSH
- Humans MeSH
- Luciferases metabolism MeSH
- RNA, Messenger genetics metabolism MeSH
- Cell Line, Tumor MeSH
- Placenta cytology drug effects metabolism MeSH
- Receptors, Calcitriol genetics metabolism MeSH
- Gene Expression Regulation, Neoplastic drug effects MeSH
- Genes, Reporter MeSH
- Retinoid X Receptor alpha genetics metabolism MeSH
- Cell Separation MeSH
- Pregnancy MeSH
- Protein Transport drug effects MeSH
- Trophoblasts cytology drug effects metabolism MeSH
- Check Tag
- Humans MeSH
- Pregnancy MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Estradiol MeSH
- Cadherins MeSH
- Calcitriol MeSH
- Luciferases MeSH
- RNA, Messenger MeSH
- Receptors, Calcitriol MeSH
- Retinoid X Receptor alpha MeSH
Vitamin D receptor (VDR) regulates the expression of many genes involved in mineral metabolism, cellular proliferation, differentiation and drug biotransformation. We studied the expression and activity of VDR and its heterodimerization partner retinoid X receptor-alpha (RXRalpha) in choriocarcinoma trophoblast cell lines BeWo and JEG-3, in comparison with human isolated placental cytotrophoblasts and human full term placenta. We found that VDR and RXRalpha are localised in the human term placenta trophoblast and expressed in isolated cytotrophoblasts. However, we found low expression and no transcriptional activity of VDR in used choriocarcinoma cell lines. The inhibitor of DNA methylation, 5-deoxy-3'-azacytidine, and histone deacetylase inhibitor sodium butyrate partially restored the expression of VDR, suggesting an epigenetic suppression of the gene in choriocarcinoma cells. Differentiation of BeWo cells resulted in up-regulation of VDR mRNA. Finally, we observed a non-genomic effect of 1,25(OH)(2)D(3) in the activation of the extracellular signal-regulated kinase (ERK) signalling pathway in JEG-3 cells. In conclusion, our results suggest an epigenetic repression of VDR gene expression and activity in choriocarcinoma cell lines, and a non-genomic effect of 1,25(OH)(2)D(3) in JEG-3 cells.
References provided by Crossref.org
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