中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/4971
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 29490/55136 (53%)
Visitors : 1512528      Online Users : 411
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
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/4971


    Title: The profile of cardiac cytochrome c oxidase (COX) expression in an accelerated cardiac-hypertrophy model
    Authors: 郭薇雯(Wei-Wen Kuo);(Chu CY);吳介信(Chieh-Hsi Wu);(Lin JA);(Liu JY);(Ying TH);李信達(Shin-Da Lee);(Hsieh YH);(Hsu HH)*;黃志揚*
    Contributors: 醫學院生物科技學系
    Keywords: cytochrome c oxidase (COX);complete coarctation;cardiac hypertrophy;genetically hypertensive rats
    Date: 2005-11
    Issue Date: 2009-08-21 11:03:43 (UTC+8)
    Abstract: The contribution of the mitochondrial components, the main source of energy for the cardiac hypertrophic growth induced by pressure overload, is not well understood. In the present study, complete coarctation of abdominal aorta was used to induce the rapid development of cardiac hypertrophy in rats. One to two days after surgery, we observed significantly higher blood pressure and cardiac hypertrophy, which remained constantly high afterwards. We found an early increased level of cytochrome c oxidase (COX) mRNA determined by in-situ hybridization and dot blotting assays in the hypertrophied hearts, and a drop to the baseline 20 days after surgery. Similarly, mitochondrial COX protein level and enzyme activity increased and, however, dropped even lower than baseline 20 days following surgery. In addition, in natural hypertension-induced hypertrophic hearts in genetically hypertensive rats, the COX protein was significantly lower than in normotensive rats. Taken together, the lower efficiency of mitochondrial activity in the enlarged hearts of long-term complete coarcted rats or genetically hypertensive rats could be, at least partially, the cause of hypertensive cardiac disease. Additionally, the rapid complete coarctation-induced cardiac hypertrophy was accompanied by a disproportionate COX activity increase, which was suggested to maintain the cardiac energy-producing capacity in overloaded hearts.
    Relation: JOURNAL OF BIOMEDICAL SCIENCE12(4):601~610
    Appears in Collections:[Department of Biological Science and Technology] Journal articles

    Files in This Item:

    File SizeFormat
    0KbUnknown444View/Open


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

     


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