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Genetic and Epigenetic Control of the Major Histocompatibility Complex Class Ib Gene HLA‐G in Trophoblast Cell Lines
Author(s) -
Holling Tjadine M.,
Bergevoet Marloes W.T.,
Wierda Rutger J.,
Van Eggermond Marja C.J.A.,
Van Den Elsen Peter J.
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04660.x
Subject(s) - ciita , biology , dna methylation , epigenetics , human leukocyte antigen , transactivation , promoter , genetics , major histocompatibility complex , histone , microbiology and biotechnology , gene , gene expression , mhc class ii , antigen
The transcriptional regulation of the major histocompatibility complex class (MHC) Ib gene HLA‐G differs from the classical MHC class I genes. The cis‐acting regulatory elements typical for classical MHC class I promoters are divergent in the promoter of HLA‐G , rendering this gene unresponsive to NF‐κB, IRF‐1, and class II transactivator (CIITA)‐mediated activation pathways. However, as we have previously shown, transactivation of HLA‐G is regulated by CREB‐1. Because CREB‐1 is ubiquitously expressed, this observation does not explain the tissue‐restricted expression of HLA‐G in extravillous cytotrophoblasts. Using HLA‐G‐expressing JEG‐3 cells and HLA‐G‐deficient JAR trophoblast‐derived choriocarcinoma cells as a model, we have investigated the contribution of DNA methylation and histone acetylation in the transcriptional activation of HLA‐G . Despite similar levels of DNA methylation both in JEG3 and JAR cells, we found the levels of histone acetylation in HLA‐G promoter chromatin to be significantly enhanced in JEG3 cells coinciding with HLA‐G expression.