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学科主题: 临床医学
题名:
14-3-3 inhibits insulin-like growth factor-I-induced proliferation of cardiac fibroblasts via a phosphatidylinositol 3-kinase-dependent pathway
作者: Qi, Jian-Yong; Xu, Ming; Lu, Zhi-Zhen; Zhang, You-Yi1
关键词: cardiac fibroblasts ; nuclear factor of activated T cells ; phosphatidylinositol 3-kinase ; proliferation ; 14-3-3 proteins
刊名: CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
发表日期: 2010-03-01
DOI: 10.1111/j.1440-1681.2009.05282.x
卷: 37, 期:3, 页:296-302
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Pharmacology & Pharmacy ; Physiology
研究领域[WOS]: Pharmacology & Pharmacy ; Physiology
关键词[WOS]: SIGNALING PATHWAYS ; HEART-FAILURE ; HYPERTROPHY ; PROTEINS ; ACTIVATION ; EXPRESSION ; CELLS ; 14-3-3-PROTEINS ; PHOSPHORYLATION ; ASSOCIATION
英文摘要:

P>1. Insulin-like growth factor (IGF)-I plays an important role in the pathogenesis of heart disease and has been shown to strongly induce the proliferation of cardiac fibroblasts (CFs). It remains unknown whether 14-3-3 proteins, which are associated the regulation of signal transduction, affect IGF-I-induced CF proliferation.

2. In the present study, we investigated the effects of 14-3-3 proteins on CF proliferation in response to IGF-I. Proliferation of CFs was determined by cell counting and a bromodeoxyuridine incorporation assay. Phosphorylation of signalling molecules was evaluated by western blottling. Activity of nuclear factor of activated T cells (NFAT) was examined using a dual luciferase reporter gene assay and immunofluorescence.

3. It was found that adenovirus-mediated transfection of YFP-R18 peptide (AdR18), a known inhibitor of 14-3-3, significantly enhanced IGF-I-induced CF proliferation. This potentiation arose from an increase in phosphorylation of phosphatidylinositol 3-kinase (PI3-K) and AKT (protein kinase B), inactivation of glycogen synthesis kinase (GSK) 3 beta and increased NFAT activity.

4. Collectively, the results of the present study suggest that 14-3-3 proteins inhibit IGF-I-induced CF proliferation via a PI3-K-dependent NFAT signalling pathway. This finding may contribute to our understanding of the function of 14-3-3 proteins in the heart.

语种: 英语
所属项目编号: 2006CB503806 ; 30672466 ; 30821001
项目资助者: Foundation of National Key Basic Research and Development Project ; National Natural Science Foundation of China
WOS记录号: WOS:000274908000008
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/56137
Appears in Collections:北京大学第三临床医学院_心血管内科_期刊论文

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作者单位: 1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing, Peoples R China
2.Peking Univ, Hosp 3, Inst Vasc Med, Beijing 100191, Peoples R China

Recommended Citation:
Qi, Jian-Yong,Xu, Ming,Lu, Zhi-Zhen,et al. 14-3-3 inhibits insulin-like growth factor-I-induced proliferation of cardiac fibroblasts via a phosphatidylinositol 3-kinase-dependent pathway[J]. CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY,2010,37(3):296-302.
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