Phosphorylation and Acetylation of Histone H3 and Autoregulation by Early Growth Response 1 Mediate Interleukin 1β Induction of Early Growth Response 1 Transcription

被引:40
|
作者
Wang, Bo [1 ,2 ]
Chen, Jinbiao [1 ]
Santiago, Fernando S.
Janes, Mary [3 ,4 ]
Kavurma, Mary M. [1 ]
Chong, Beng H. [1 ]
Pimanda, John E. [3 ,4 ]
Khachigian, Levon M. [1 ]
机构
[1] Univ New S Wales, Ctr Vasc Res, Sydney, NSW 2052, Australia
[2] Qiqihar Med Univ, Qiqihar, Peoples R China
[3] Univ New S Wales, Fac Med, Canc Res Ctr, Sydney, NSW 2052, Australia
[4] Univ New S Wales, Fac Med, Prince Wales Clin Sch, Sydney, NSW 2052, Australia
基金
英国医学研究理事会;
关键词
histone modification; immediate-early gene; transcription; SMOOTH-MUSCLE-CELLS; FACTOR EGR-1; ENDOTHELIAL-CELLS; GENE-EXPRESSION; FACTOR-I; TUMOR-GROWTH; KAPPA-B; DIFFERENTIATION; ACTIVATION; INJURY;
D O I
10.1161/ATVBAHA.109.193821
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective-The transcription factor early growth response (EGR)-1 has been implicated as a key vascular phenotypic switch through its control of inducible transcription. EGR-1 autoregulation, and histone modification in the EGR-1 promoter, represent key mechanisms in EGR-1 control, but have not been explored. Methods and Results-We demonstrate that EGR-1 regulates its own transcription and that this involves histone H3 phosphorylation and acetylation. EGR-1 transactivates its promoter in smooth muscle cells exposed to interleukin (IL) 1 beta through a novel cis-acting element (-211/-203). PD98059, which inhibits mitogen-activated protein kinase kinase/extracellular regulated kinase (MEK/ERK) attenuates IL-1 beta-inducible phosphorylation of extracellular signal-regulated kinase 1/2 and mitogen and stress-activated protein kinases 1/2; and reduces levels of phosphorylated and acetylated histone H3. Histone deacetylase inhibition enhances EGR-1 transcription in response to cytokine. Conversely, suppression of histone modification with mitogen and stress-activated protein kinase 1/2 short interfering RNA, or the histone H3 acetyltransferase inhibitor Garcinol, inhibits IL-1 beta-inducible EGR-1 transcription. EGR-1 interacts with the acetyltransferase p300. Acetylated H3 and phosphorylated H3 are enriched at the promoter of EGR-1; and EGR-1 is enriched at the promoters of tissue factor and plasminogen activator inhibitor 1 in response to IL-1 beta, and attenuated by PD98059, Garcinol, and mitogen and stress-activated protein kinase 1/2 short interfering RNA. Conclusion-IL-1 beta induction of EGR-1 transcription involves histone H3 phosphorylation, acetylation, and autoregulation by EGR-1. (Arterioscler Thromb Vasc Biol. 2010;30:536-545.)
引用
收藏
页码:536 / U374
页数:16
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