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Neoplasma Vol.54, p.455-462, 2007 |
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Title: Modulation of HLA-G expression | ||
Author: K. POLAKOVA, E. BANDZUCHOVA, J. TIRPAKOVA, D. KUBA, G. RUSS | ||
Abstract: Recent studies demonstrated that HLA-G transcription is in some cells silenced by epigenetic mechanisms as DNA
methylation and histone modification. Accordingly HLA-G gene transcriptions can be activated in such cells by demethylating
agent or by inhibitors of histone deacetylation. In addition to epigenetic alterations HLA-G gene transcription can be activated
by stress. In the present study these aspects of HLA-G expression are re-examined and a new inhibitor of histone deacetylation
(valproic acid) and hypoxia mimetic chemical (CoCl2) are included. The highest activation of HLA-G transcription was
achieved by treatment of choriocarcinoma JAR and lymphoblastoid RAJI cell lines with demethylating agent 5-aza-2´-
deoxycytidine. Treatment of JAR and RAJI cells with histone deacetylase inhibitors (sodium butyrate and valproic acid)
also enhanced HLA-G transcription. Nevertheless this increase in HLA-G expression was low as compared with activation
by 5-aza-2´- deoxycytidine. The hypoxia mimetic agents (desferrioxamine or CoCl2) had no detectable effect on HLA-G
gene transcription in examined cells. Relatively high increase of HLA-G transcription was detected in JAR and RAJI cells
exposed to heat shock treatment. Interestingly heat shock induced high expression of HLA-G6 transcript in JAR cells. Heat
shock treatment had no effect on alternative splicing of constitutively expressed HLA-G mRNA in choriocarcinoma cell line
JEG-3. HLA-G1 protein expression was induced in JAR and RAJI cell lines by 5-aza-2´- deoxycytidine. In agreement with
the differences in the levels of HLA-G transcripts JAR cells express more of HLA-G1 protein than RAJI cells. |
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Keywords: HLA-G; demethylation; histone deacetylation; hypoxia; heat shock | ||
Year: 2007, Volume: 54, Issue: | Page From: 455, Page To: 462 | |
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