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学科主题: 基础医学
题名:
GATA4 regulates ANF expression synergistically with Sp1 in a cardiac hypertrophy model
作者: Hu, Xiaoqing1; Li, Tao2; Zhang, Chenguang1; Liu, Yinan1; Xu, Ming3,4; Wang, Weiping1,4; Jia, Zhuqing1,4; Ma, Kangtao1,4; Zhang, Youyi3,4; Zhou, Chunyan1,4
关键词: GATA4 ; Sp1 ; Sp3 ; ANF expression ; cardiac hypertrophy ; transcription
刊名: JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
发表日期: 2011-09-01
DOI: 10.1111/j.1582-4934.2010.01182.x
卷: 15, 期:9, 页:1865-1877
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cell Biology ; Medicine, Research & Experimental
研究领域[WOS]: Cell Biology ; Research & Experimental Medicine
关键词[WOS]: TRANSCRIPTION FACTOR GATA-4 ; ACTIVATED PROTEIN-KINASES ; SERUM RESPONSE FACTOR ; HEART TUBE FORMATION ; GENE-EXPRESSION ; VENTRAL MORPHOGENESIS ; SIGNALING PATHWAY ; SP-FAMILY ; CARDIOMYOCYTES ; PHOSPHORYLATION
英文摘要:

Cardiac hypertrophy in response to multiple stimuli has important physiological and pathological significances. GATA4 serves as a nuclear integrator of several signalling pathways during cardiac hypertrophy. Sp1 and Sp3 are also reported to be involved in this process. However, the mechanism by which GATA4 acts as a mediator, integrating these ubiquitously expressed transcriptional factors, is poorly understood. We found that the expression of GATA4 and Sp1 was up-regulated in the myocardium of a pressure overload hypertrophy rat model, as well in phenylephrine-induced (PE-induced) hypertrophic growth of neonatal cardiomyocytes. GST pull-down assays demonstrated that GATA4 could interact with Sp1 in vitro. Therefore, we proposed that GATA4 cooperates with Sp1 in regulating ANF expression, as its reactivation is closely linked with hypertrophy. Further studies demonstrated that GATA4 could activate the ANF promoter synergistically with Sp1 through direct interaction. In contrast, Sp3 exhibited antagonistic function, and overexpression of Sp3 repressed the transcriptional synergy between Sp1 and GATA4. We also found that Sp1 alone could activate the ANF promoter in cardiomyocytes, whereas Sp3 exerted negative effects on ANF expression. Bioinformatics analysis revealed novel Sp-binding sites on the ANF promoter. The recruitment of GATA4 and Sp1 on the ANF promoter was enhanced during phenylephrine-mediated hypertrophy, whereas the recruitment of Sp3 was reduced. The phosphorylation of GATA4 by ERK1/2 kinase could enhance the affinity between GATA4 and Sp1. Thus, our findings revealed the critical interaction of GATA4 and Sp1 in modulating ANF expression, indicating their involvement in cardiac hypertrophy.

语种: 英语
所属项目编号: 30871253 ; 90919022 ; B07001
项目资助者: National Natural Sciences Foundation of China ; 111 Project of China
WOS记录号: WOS:000294597400007
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/60035
Appears in Collections:基础医学院_期刊论文

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作者单位: 1.Peking Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Beijing 100191, Peoples R China
2.Zhejiang Normal Univ, Dept Biol, Coll Chem & Life Sci, Jinhua, Zhejiang, Peoples R China
3.Peking Univ, Hosp 3, Inst Vasc Med, Beijing 100191, Peoples R China
4.Peking Univ, Minist Educ China, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China

Recommended Citation:
Hu, Xiaoqing,Li, Tao,Zhang, Chenguang,et al. GATA4 regulates ANF expression synergistically with Sp1 in a cardiac hypertrophy model[J]. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,2011,15(9):1865-1877.
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