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
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.