English  |  正體中文  |  简体中文  |  Items with full text/Total items : 90074/105197 (86%)
Visitors : 7160628      Online Users : 57
RC Version 6.0 © 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


    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/79909


    Title: Gelsolin;GSN) induces cardiomyocyte hypertrophy and BNP expression via p38 signaling and GATA-4 transcriptional factor activation.
    Authors: Hu, Wei-Syun;Hu, Wei-Syun;Tsung-Jung, H;Ho, Tsung-Jung;白培英;Pai, Pei-Ying;Chun, Li-Chin;Chung, Li-Chin;Kuo, Chia-Hua;Kuo, Chia-Hua;Sheng-Huang;Chang, Sheng-Huang;蔡輔仁;Tsai, Fuu-Jen;Jie, 蔡長海、Yu-Chi;Jie, Yu-Chi;Li, Ying-Ming;Liou, Ying-Ming;黃志揚;*、, CHIH-YANG HUANG
    Contributors: 生物科技學系
    Date: 2014
    Issue Date: 2014-07-03 15:41:47 (UTC+8)
    Abstract: 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 β-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.
    Relation: MOLECULAR AND CELLULAR BIOCHEMISTRY;390(1-2):263-70.
    Appears in Collections:[生物科技學系] 期刊論文

    Files in This Item:

    There are no files associated with this item.



    All items in ASIAIR are protected by copyright, with all rights reserved.


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