文化大學機構典藏 CCUR:Item 987654321/29135
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 46867/50733 (92%)
Visitors : 11887260      Online Users : 756
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: https://irlib.pccu.edu.tw/handle/987654321/29135


    Title: The novel regulations of MEF2A, CAMKK2, CALM3, and TNNI3 in ventricular hypertrophy induced by arsenic exposure in rats
    Authors: Phan, Nam Nhut
    Wang, Chih-Yang
    Lin, Yen-Chang
    Contributors: 生科所
    Keywords: Arsenic
    Cardiac function
    Hypertension
    Ventricular hypertrophy
    Date: 2014-10-03
    Issue Date: 2015-01-20 10:32:26 (UTC+8)
    Abstract: Arsenic is a ubiquitous toxic compound that exists naturally in many sources such as soil, groundwater, and food; in which vast majority forms are arsenite (As3+) or arsenate (As5+). The mechanism of arsenic detoxification in humans still remains obscured. Epidemiologic studies documented that arsenic pollution caused black foot disease, cardiovascular diseases (hypertension, hypotension, cardiomyopathy), bladder cancer and skin cancer in many countries in which Taiwan is considered as high arsenic exposure country for long time ago. However, the effects of arsenic to cardiac functions still lacked of investigation while some studies mainly focus on inflammatory and cancer mechanisms. In the present study, we found cardiac hypertrophy signaling may be the most significant pathway for up regulated genes in arsenic exposed patients via bioinformatics approach. To verify our bioinformatics prediction, arsenic was fed orally to rats at different concentration based on previous studies in Taiwan. Using hemodynamic method as the main tool to measure the changes in blood pressure, left ventricular pressure and left ventricular contractility index, the findings suggest that highly exposure to arsenic lead to hypertension; elevated left ventricular diastolic pressure and alteration in cardiac contractility which are supposed to be the interaction between arsenic and cardiac nerves activity via the changing in calcium homeostasis. Collectively, based on our real-time PCR and western blot data strongly suggest that calcium homeostasis may also go through MEF2A, TNNI3, CAMKK2, CALM3 and cardiac hypertrophy relative signaling pathway. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
    Relation: TOXICOLOGY 卷: 324 頁碼: 123-135
    Appears in Collections:[Graduate Institute of Biotechnology ] journal articles

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML336View/Open


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


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