Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/28584
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 18272/20499 (89%)
Visitors : 16051934      Online Users : 1869
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://ir.cnu.edu.tw/handle/310902800/28584


    题名: Gelsolin (GSN) induces cardiomyocyte hypertrophy and BNP expression via p38 signaling and GATA-4 transcriptional factor activation
    作者: Hu, Wei-Syun
    Ho, Tsung-Jung
    Pai, Peiying
    Chung, Li-Chin
    Kuo, Chia-Hua
    Chang, Sheng-Huang
    Tsai, Fuu-Jen
    Tsai, Chang-Hai
    Jie, Yu-Chi
    Liou, Ying-Ming
    Huang, Chih-Yang
    贡献者: 醫務管理系
    关键词: Cardiac hypertrophy
    Gelsolin ( GSN)
    Cytoskeleton
    日期: 2014-05
    上传时间: 2015-05-06 21:21:32 (UTC+8)
    出版者: Springer
    摘要: Cardiomyocyte hypertrophy is an adaptive response of the heart to various types of stress. During the period of stress accumulation, the transition from physiological hypertrophy to pathological hypertrophy results in the promotion of heart failure. Gelsolin (GSN) is a member of the actin-binding proteins, which regulate dynamic actin filament organization by severing and capping. Moreover, GSN also regulates cell morphology, differentiation, movement, and apoptosis. In this study, we used H9c2 and H9c2-GSN stable clones in an attempt to understand the mechanisms of GSN overexpression in cardiomyocytes. These data showed that the overexpression of GSN in H9c2-induced cardiac hypertrophy and increased the pathological hypertrophy markers atrial natriuretic peptide brain natriuretic peptide. Furthermore, we found that E-cadherin expression decreased with the overexpression of GSN in H9c2, but beta-catenin expression increased. These data presume that the cytoskeleton is loose. Further, previous studies show that the mitogen-activated protein kinase pathway can induce cardiac hypertrophy. Our data showed that p-p38 expression increased with the overexpression of GSN in H9c2, and the transcription factor p-GATA4 expression also increased, suggesting that the overexpression of GSN in H9c2-induced cardiac hypertrophy seemed to be regulated by the p38/GATA4 pathway. Moreover, we used both the p38 inhibitor (SB203580) and GSN siRNA to confirm our conjecture. We found that both of these factors significantly suppressed gelsolin-induced cardiac hypertrophy through p38/GATA4 signaling pathway. Therefore, we predict that the gene silencing of GSN and/or the downstream blocking of GSN along the p38 pathway could be applied to ameliorate pathological cardiac hypertrophy in the future.
    關聯: Molecular and Cellular Biochemistry, v.390 n.1-2, pp.263-270
    显示于类别:[Dept. of Hospital and Health (including master's program)] Periodical Articles

    文件中的档案:

    档案 描述 大小格式浏览次数
    index.html0KbHTML2375检视/开启


    在CNU IR中所有的数据项都受到原著作权保护.

    TAIR相关文章

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback