Document Detail

Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice.
MedLine Citation:
PMID:  20081106     Owner:  NLM     Status:  MEDLINE    
Tenascin-C (TN-C) is an extracellular matrix glycoprotein with high bioactivity. It is expressed at low levels in normal adult heart, but upregulated under pathological conditions, such as myocardial infarction (MI). Recently, we (Ref. 34) reported that MI patients with high serum levels of TN-C have a greater incidence of maladaptive cardiac remodeling and a worse prognosis. We hypothesized that TN-C may aggravate left ventricular remodeling. To examine the effects of TN-C, MI was induced by ligating coronary arteries of TN-C knockout (KO) mice under anesthesia and comparing them with sibling wild-type (WT) mice. In WT+MI mice, TN-C expression was upregulated at day 1, peaked at day 5, downregulated and disappeared by day 28, and the molecule was localized in the border zone between intact myocardium and infarct lesions. The morphometrically determined infarct size and survival rate on day 28 were comparable between the WT+MI and KO+MI groups. Echocardiography and hemodynamic analyses demonstrated left ventricular end-diastolic diameter, myocardial stiffness, and left ventricular end-diastolic pressure to be significantly increased in both WT+MI and KO+MI mice compared with sham-operated mice. However, end-diastolic pressure and dimension and myocardial stiffness of KO+MI were lower than those of the WT+MI mice. Histological examination revealed normal tissue healing, but interstitial fibrosis in the residual myocardium in peri-infarcted areas was significantly less pronounced in KO+MI mice than in WT+MI mice. TN-C may thus accelerate adverse ventricular remodeling, cardiac failure, and fibrosis in the residual myocardium after MI.
Tomohiro Nishioka; Katsuya Onishi; Naoshi Shimojo; Yuka Nagano; Hidenori Matsusaka; Masaki Ikeuchi; Tomomi Ide; Hiroyuki Tsutsui; Michiaki Hiroe; Toshimichi Yoshida; Kyoko Imanaka-Yoshida
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-15
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  298     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-02-25     Completed Date:  2010-04-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1072-8     Citation Subset:  IM    
Dept. of Pathology and Matrix Biology, Mie Univ. Graduate School of Medicine, Tsu, Japan.
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MeSH Terms
Disease Models, Animal
Mice, Inbred BALB C
Mice, Knockout
Myocardial Infarction / physiopathology*
Signal Transduction / physiology
Smad3 Protein / physiology
Tenascin / genetics,  physiology*
Transforming Growth Factor beta / physiology
Ventricular Dysfunction, Left / physiopathology*
Ventricular Remodeling / physiology*
Reg. No./Substance:
0/Smad3 Protein; 0/Smad3 protein, mouse; 0/Tenascin; 0/Transforming Growth Factor beta

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

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