CHANGES IN EXTRACELLULAR-MATRIX COMPONENTS IN CARDIOMYOPATHIC SYRIAN-HAMSTER, BIO-14.6

Citation
K. Nogami et al., CHANGES IN EXTRACELLULAR-MATRIX COMPONENTS IN CARDIOMYOPATHIC SYRIAN-HAMSTER, BIO-14.6, Japanese Circulation Journal, 59(9), 1995, pp. 631-640
Citations number
43
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00471828
Volume
59
Issue
9
Year of publication
1995
Pages
631 - 640
Database
ISI
SICI code
0047-1828(1995)59:9<631:CIECIC>2.0.ZU;2-3
Abstract
We examined changes in the distribution of extracellular matrix compon ents in the myocardium of cardiomyopathic Syrian hamsters (BIO 14.6). Fibronectin, laminin, and type IV collagen, and type I and III collage ns were immunohistochemically stained by the avidin-biotin-peroxidase complex method, using a polyclonal antibody for each component. Hearts obtained from 4 stages of BIO 14.6 cardiomyopathy were examined. Peri - and endomysial fibrosis increased as the disease progressed. Replace ment and meshwork (perimysial fibrosis penetrating the intercellular s pace) fibrotic lesions appeared beginning in the 2nd stage, ie, the fi brotic and healing stage. All of the components examined, ie, fibronec tin, laminin and type IV collagen, and type I and III collagens, were present in various fibrotic lesions and played a significant role in f ibrotic changes throughout all of the stages of the disease. No primar y deficit of any of these components was seen. An increased distributi on of fibronectin was observed in both the enlarged peri- and endomysi al spaces beginning in the initial stage, ie, the necrotic stage, when myocyte hypertrophy was inconspicuous, and distribution throughout th e myocardium increased further as the disease progressed. Laminin and type IV collagen in the fibrotic lesions were not restricted to the my ocyte membrane. Type III collagen was distributed in replacement and m eshwork fibrotic lesions, and the extent of its distribution increased in proportion to that of type I collagen. The continuous increases in the distribution of fibronectin, laminin and type III collagen indica te that fibrotic changes occurred continuously in this model. The depo sition of type I and III collagens and fibronectin before myocyte hype rtrophy suggests that the fibrotic changes in this model were not rela ted to myocyte hypertrophy in the early stage.