Document Detail


Role of microtubules in the contractile dysfunction of myocytes from tachycardia-induced dilated cardiomyopathy.
MedLine Citation:
PMID:  9618245     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Microtubules of cardiac myocytes are increased in pressure-overloaded cardiac hypertrophy, which interfere with the actin-myosin crossbridge motion and depress muscle contractility. However, it is unknown whether microtubules are increased in non-hypertrophied, dilated cardiomyopathy and, if so, their increase could contribute to the depressed contractility. We assessed the contractile function of isolated left-ventricular (LV) myocytes and also quantitated tubulin mRNA levels as well as free and polymerized tubulin proteins using the LV myocardium obtained from dogs with rapid pacing (240 beats/min, 4 weeks)-induced dilated failing cardiomyopathy (HF; n = 6) and control dogs (n = 6). Myocyte contractility was significantly depressed in HF compared to control. Northern blot analysis indicated that tubulin mRNA levels (normalized to GAPDH mRNA) in HF dogs were upregulated (0.43 +/- 0.04 v 0.13 +/- 0.02; P < 0.01). In contrast, the amount of total tubulins (633 +/- 52 v 697 +/- 42 micrograms/g wet weight; P = N.S.) and the ratio of polymerized tubulin fraction-to-total tubulin (0.44 +/- 0.02 v 0.44 +/- 0.01; P = N.S.) did not differ between the two groups. Immunohistochemical studies showed no apparent differences in the distribution or density of intracellular microtubule network. Further, the exposure of myocytes to colchicine (1 mumol/l, 30 min), which depolymerizes microtubules, did not promote any improvement of the depressed myocyte contraction. Pacing-induced tachycardia increased myocardial tubulin mRNA, but the amount of total and polymerized tubulins were not increased, indicating that alterations in myocyte microtubules do not contribute to the contractile abnormalities in this model of HF.
Authors:
M Takahashi; H Tsutsui; S Kinugawa; K Igarashi-Saito; S Yamamoto; M Yamamoto; H Tagawa; K Imanaka-Yoshida; K Egashira; A Takeshita
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  30     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1998 May 
Date Detail:
Created Date:  1998-09-17     Completed Date:  1998-09-17     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1047-57     Citation Subset:  IM    
Affiliation:
Research Institute of Angiocardiology, Kyushu University School of Medicine, Fukuoka, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Biopolymers
Cardiomyopathy, Dilated / etiology,  physiopathology*
Colchicine / pharmacology
Dogs
Microtubules / physiology*
Myocardial Contraction / physiology*
Myocardium / pathology*
RNA, Messenger / analysis
Tachycardia / complications,  physiopathology*
Tubulin / analysis,  genetics
Ventricular Dysfunction, Left / physiopathology*
Chemical
Reg. No./Substance:
0/Biopolymers; 0/RNA, Messenger; 0/Tubulin; 64-86-8/Colchicine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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