Critical Role of Histone Acetylation by p300 in Human Placental 11β-HSD2 Expression
Author(s) -
Jianneng Li,
Wangsheng Wang,
Chao Liu,
Weihua Wang,
Wenjiao Li,
Qun Shu,
ZiJiang Chen,
Kang Sun
Publication year - 2013
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2012-4291
Subject(s) - syncytiotrophoblasts , chromatin immunoprecipitation , gene knockdown , acetylation , histone , immunoprecipitation , biology , hdac4 , p300 cbp transcription factors , sap30 , microbiology and biotechnology , transcription factor , histone h3 , placenta , histone h2a , gene expression , biochemistry , promoter , histone acetyltransferases , fetus , genetics , apoptosis , gene , pregnancy
Fetal overexposure to glucocorticoids leads to growth restriction. Optimal fetal glucocorticoid level is ensured by the expression of cortisol-inactivating enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in placental syncytiotrophoblasts. The transcription factor selective promoter factor 1 (Sp1) is known to up-regulate 11β-HSD2 expression in the presence of enhanced histone acetylation in syncytiotrophoblasts, but the mechanisms underlying histone acetylation remain unknown.
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