Document Detail


Embryonic smooth muscle myosin heavy chain SMemb is expressed in pressure-overloaded cardiac fibroblasts.
MedLine Citation:
PMID:  10737564     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Left ventricular hypertrophy (LVH) is a secondary adaptation to increased external load. Various qualitative and quantitative changes in myocytes and extracellular components occur during the development of LVH. It has recently been demonstrated that alpha-smooth muscle actin (alpha-SMA)-expressing myofibroblasts appear in the interstitium of the heart subjected to increased workload suggesting that cardiac fibroblasts as well as myocytes alter their phenotype in response to pressure overload. In the present study, to explore the load-induced response and phenotypic modulation of cardiac fibroblasts, the localization of embryonic smooth muscle myosin heavy chain (SMemb) and alpha-SMA in thoracic aorta-constricted rat hearts was investigated by immunohistochemistry, and the morphology of the SMemb-expressing cells was examined by electron microscopy. In addition, to clarify the mechanisms by which SMemb is induced in pressure-overloaded hearts, mRNA expression of SMemb in aorta-constricted rat hearts and in transforming growth factor-beta1 (TGF-beta1)-treated or mechanically-stretched cultured cardiac fibroblasts was investigated. Enhanced staining of SMemb and alpha-SMA was detected in the interstitial spindle-shaped cells in the fibrotic lesions of the pressure-overloaded left ventricles by immunohistochemistry. These cells were demonstrated by electron microscopy to have features specific for activated fibroblasts such as serrated nuclei or prominent rough endoplasmic reticulum. These cells also had characteristic features of myofibroblasts, i.e. irregularly arranged actin filaments and scattered dense bodies. Northern blot analysis revealed increased mRNA levels of SMemb both in aorta-constricted rat hearts and in cultured cardiac fibroblasts stimulated by TGF-beta1 or by mechanical stretch. These results suggest that SMemb may be a molecular marker both for the detection of activated cardiac fibroblasts that may play important roles in the remodeling of pressure-overloaded cardiac interstitium, and for the identification of the regu latory mechanisms that control the phenotypic modulation of cardiac fibroblasts in response to pressure overload.
Authors:
I Shiojima; M Aikawa; J Suzuki; Y Yazaki; R Nagai
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Japanese heart journal     Volume:  40     ISSN:  0021-4868     ISO Abbreviation:  Jpn Heart J     Publication Date:  1999 Nov 
Date Detail:
Created Date:  2000-04-20     Completed Date:  2000-04-20     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0401175     Medline TA:  Jpn Heart J     Country:  JAPAN    
Other Details:
Languages:  eng     Pagination:  803-18     Citation Subset:  IM    
Affiliation:
Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, Japan.
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MeSH Terms
Descriptor/Qualifier:
Actins / metabolism*
Animals
Fibroblasts / metabolism*
Fibrosis
Hypertrophy, Left Ventricular / pathology,  physiopathology*
Immunohistochemistry
Male
Muscle, Smooth / embryology*,  metabolism
Myocardium / metabolism,  pathology*
Myosin Heavy Chains / metabolism*
Pressure
RNA, Messenger / metabolism
Rats
Rats, Wistar
Chemical
Reg. No./Substance:
0/Actins; 0/Myosin Heavy Chains; 0/RNA, Messenger

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


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