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学科主题临床医学
Inhibitory effect of 14-3-3 proteins on serum-induced proliferation of cardiac fibroblasts
Du, JH; Liao, WQ; Wang, YY; Han, CD; Zhang, YY
关键词proliferation 14-3-3 R18 peptide cardiac fibroblasts ERK GSK3 beta NFATc3
刊名EUROPEAN JOURNAL OF CELL BIOLOGY
2005-10-01
DOI10.1016/j.ejcb.2005.06.006
84期:10页:843-852
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology
研究领域[WOS]Cell Biology
关键词[WOS]SYNTHASE KINASE 3-BETA ; SMOOTH-MUSCLE-CELLS ; PHOSPHATIDYLINOSITOL 3-KINASE ; GENE-EXPRESSION ; A(2B) RECEPTORS ; ANGIOTENSIN-II ; DNA-SYNTHESIS ; GROWTH-FACTOR ; ACTIVATION ; RATS
英文摘要

Proliferation in cardiac fibroblasts (CFs) can be induced by a wide variety of growth factors that recruit multiple signal transduction pathways, including mitogen-activated protein kinase, phosphatidylinositol 3-kinase and protein kinase C. As a family of dimeric phophoserine-binding proteins, 14-3-3s are associated with a multitude of proteins that regulate signal transduction, apoptosis and checkpoint control pathways. However, it remains unknown whether the 14-3-3 proteins play an active role in cardiac proliferation and alter their expression patterns in response to growth factors in CFs. R18 peptide, an isoform-independent 14-3-3 inhibitor, was used to disrupt 14-3-3 function by adenovirus-mediated transfer of R18-EYFP (AdR18). Our results demonstrate that the 14-3-3 isoforms gamma, zeta and epsilon were highly expressed in CFs and the expression of 14-3-3 epsilon was elevated following serum stimulation. Inhibition of 14-3-3 proteins by AdR18 potentiated mitogen-induced DNA synthesis in CFs. This potentiation was presumably due to the increased inactivated glycogen synthase kinase-3 beta by Ser9 phosphorylation and nuclear factor of activated T-cell nuclear accumulation. However, AdR18 had no effect on extracellular signal-regulated kinase phosphorylation and reduced p70 S6 kinase (p70S6K) phosphorylation upon mitogenic stimulation. Furthermore, though R18 can block 14-3-3 binding abilities, it did not affect the serum-induced upregulation of 14-3-3 epsilon protein. Collectively, these findings reveal that the expression of 14-3-3 epsilon can be upreglulated by serum in CFs and 14-3-3s may exert an inhibitory effect on serum-induced proliferation. (c) 2005 Elsevier GmbH. All rights reserved.

语种英语
WOS记录号WOS:000233197400005
引用统计
被引频次:11[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/400002259/64874
专题北京大学第三临床医学院_心血管内科
作者单位1.Peking Univ, Inst Vasc Med, Minist Educ, Hosp 3, Beijing 100083, Peoples R China
2.Peking Univ, Inst Vasc Med, Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100083, Peoples R China
推荐引用方式
GB/T 7714
Du, JH,Liao, WQ,Wang, YY,et al. Inhibitory effect of 14-3-3 proteins on serum-induced proliferation of cardiac fibroblasts[J]. EUROPEAN JOURNAL OF CELL BIOLOGY,2005,84(10):843-852.
APA Du, JH,Liao, WQ,Wang, YY,Han, CD,&Zhang, YY.(2005).Inhibitory effect of 14-3-3 proteins on serum-induced proliferation of cardiac fibroblasts.EUROPEAN JOURNAL OF CELL BIOLOGY,84(10),843-852.
MLA Du, JH,et al."Inhibitory effect of 14-3-3 proteins on serum-induced proliferation of cardiac fibroblasts".EUROPEAN JOURNAL OF CELL BIOLOGY 84.10(2005):843-852.
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