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Role of histone deacetylation in cell-specific expression of endothelial nitric-oxide synthase
Gan, YH; Shen, YH; Wang, J; Wang, XW; Utama, B; Wang, J; Wang, XL
刊名JOURNAL OF BIOLOGICAL CHEMISTRY
2005-04-22
DOI10.1074/jbc.M412960200
280期:16页:16467-16475
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology
研究领域[WOS]Biochemistry & Molecular Biology
关键词[WOS]REPRESS TRANSCRIPTION ; GENE-EXPRESSION ; DNA METHYLATION ; BINDING PROTEIN ; SP1 SITE ; PROMOTER ; INHIBITORS ; ACETYLATION ; COMPLEX ; HTERT
英文摘要

Histone acetylation plays an important role in chromatin remodeling and gene expression. The molecular mechanisms involved in cell-specific expression of endothelial nitric-oxide synthase ( eNOS) are not fully understood. In this study we investigated whether histone deacetylation was involved in repression of eNOS expression in non-endothelial cells. Induction of eNOS expression by histone deacetylase ( HDAC) inhibitors trichostatin A (TSA) and sodium butyrate was observed in all four different types of non-endothelial cells examined. Chromatin immunoprecipitation assays showed that the induction of eNOS expression by TSA was accompanied by a remarkable increase of acetylation of histone H3 associated with the eNOS 5′-flanking region in the non-endothelial cells. Moreover, DNA methylation-mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2′-deoxycytidine (AzadC) synergistically induced eNOS expression in non-endothelial cells. The proximal Sp1 site is critical for basal activity of eNOS promoter. The induction of eNOS by inhibition of HDACs in non-endothelial cells, however, appeared not mediated by the changes in Sp1 DNA binding activity. We further showed that Sp1 bound to the endogenous eNOS promoter and associated with HDAC1 in non-endothelial HeLa cells. Combined TSA and AzadC treatment increased Sp1 binding to the endogenous eNOS promoter but decreased the association between HDAC1 and Sp1 in HeLa cells. Our data suggest that HDAC1 plays a critical role in eNOS repression, and the proximal Sp1 site may serve a key target for HDCA1-mediated eNOS repression in non-endothelial cells.

语种英语
WOS记录号WOS:000228444800121
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被引频次:69[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/59728
专题北京大学口腔医学院
作者单位1.Baylor Coll Med, Michael E DeBakey Dept Surg, Div Cardiothorac Surg, Houston, TX 77030 USA
2.Peking Univ, Sch Stomatol, Ctr TMJ Disorders, Beijing 100081, Peoples R China
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Gan, YH,Shen, YH,Wang, J,et al. Role of histone deacetylation in cell-specific expression of endothelial nitric-oxide synthase[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2005,280(16):16467-16475.
APA Gan, YH.,Shen, YH.,Wang, J.,Wang, XW.,Utama, B.,...&Wang, XL.(2005).Role of histone deacetylation in cell-specific expression of endothelial nitric-oxide synthase.JOURNAL OF BIOLOGICAL CHEMISTRY,280(16),16467-16475.
MLA Gan, YH,et al."Role of histone deacetylation in cell-specific expression of endothelial nitric-oxide synthase".JOURNAL OF BIOLOGICAL CHEMISTRY 280.16(2005):16467-16475.
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