EXTRACELLULAR-MATRIX COMPONENTS IN DILATED CARDIOMYOPATHY - IMMUNOHISTOCHEMICAL STUDY OF ENDOMYOCARDIAL BIOPSY SPECIMENS

Citation
K. Nogami et al., EXTRACELLULAR-MATRIX COMPONENTS IN DILATED CARDIOMYOPATHY - IMMUNOHISTOCHEMICAL STUDY OF ENDOMYOCARDIAL BIOPSY SPECIMENS, Japanese Heart Journal, 37(4), 1996, pp. 483-494
Citations number
26
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00214868
Volume
37
Issue
4
Year of publication
1996
Pages
483 - 494
Database
ISI
SICI code
0021-4868(1996)37:4<483:ECIDC->2.0.ZU;2-E
Abstract
Fibrotic change is one of the characteristic features of the heart wit h idiopathic dilated cardiomyopathy (DCM), but the extracellular matri x components have not been fully clarified. Fibronectin, laminin, and types TV, I and III collagen staining using the avidin-biotin-peroxida se complex method was conducted to study the localization of extracell ular matrix components in biopsy specimens obtained from 7 patients wi th DCM. Fibronectin was observed in the endomysium and perimysium, co- existent with types I and III collagen; it was also distributed nonhom ogeneously in the replacement fibrotic lesions. The staining intensity in a section varied substantially from location to location. Laminin surrounded the myocytes and was distributed in the endomysium localize d together with type TV collagen, but it was not found in the perimysi um. Weak but positive staining was observed in replacement fibrotic le sions in 2 patients. Similarly to laminin, type ni collagen staining w as observed around the myocytes and in the endomysium. It was also obs erved in replacement fibrotic lesions in 4 patients either with or wit hout laminin. Type I collagen, localized together with type III collag en, was distributed in both the endomysium and perimysium. It was also distributed nonhomogeneously in the replacement fibrotic lesions. Sim ilar staining to type I collagen was seen for type III collagen. In su mmary, all examined components were observed in the fibrotic lesions w ith no primary deficit of any examined component being demonstrated. T he variability of staining intensity and positive fibronectin staining suggests that the phases of fibrotic changes differed substantially f rom location to location.