IR@PKUHSC  > 北京大学第三临床医学院  > 心血管内科
学科主题临床医学
14-3-3 inhibits insulin-like growth factor-I-induced proliferation of cardiac fibroblasts via a phosphatidylinositol 3-kinase-dependent pathway
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
2010-03-01
DOI10.1111/j.1440-1681.2009.05282.x
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
WOS记录号WOS:000274908000008
项目编号2006CB503806 ; 30672466 ; 30821001
资助机构Foundation of National Key Basic Research and Development Project ; National Natural Science Foundation of China
引用统计
被引频次:5[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/400002259/56137
专题北京大学第三临床医学院_心血管内科
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
推荐引用方式
GB/T 7714
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.
APA Qi, Jian-Yong,Xu, Ming,Lu, Zhi-Zhen,&Zhang, You-Yi.(2010).14-3-3 inhibits insulin-like growth factor-I-induced proliferation of cardiac fibroblasts via a phosphatidylinositol 3-kinase-dependent pathway.CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY,37(3),296-302.
MLA Qi, Jian-Yong,et al."14-3-3 inhibits insulin-like growth factor-I-induced proliferation of cardiac fibroblasts via a phosphatidylinositol 3-kinase-dependent pathway".CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY 37.3(2010):296-302.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Qi, Jian-Yong]的文章
[Xu, Ming]的文章
[Lu, Zhi-Zhen]的文章
百度学术
百度学术中相似的文章
[Qi, Jian-Yong]的文章
[Xu, Ming]的文章
[Lu, Zhi-Zhen]的文章
必应学术
必应学术中相似的文章
[Qi, Jian-Yong]的文章
[Xu, Ming]的文章
[Lu, Zhi-Zhen]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。