Abstract
The tight-skin (TSK) mouse, a possible animal model for scleroderma, has multiple abnormalities including increased dermal thickness, cardiomegaly, emphysematous lungs, and an enlarged skeleton. Previous investigations have demonstrated an increased collagen and glycosaminoglycan (GAG) content in the skin and lungs of these mice. The present correlative investigation of the biochemical and ultrastructural properties of the heart in the TSK mouse also revealed an increased presence of collagen. Analysis of collagen types in the TSK heart showed there was a shift in the ratio of type I: type III: type V from the normal values. Over 90% of the collagen was type I, while both types III and V were decreased in this organ. The ultrastructural examination of the left ventricle demonstrated extensive accumulations of perivascular and intercellular edema fluid, foci of myocytolysis, and areas of moderately increased collagen deposits within interstitial sites. These findings suggest that an increased collagen deposition (type 1) may be a contributing factor to cardiac enlargement in the TSK mouse.
Original language | English (US) |
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Pages (from-to) | 581-587 |
Number of pages | 7 |
Journal | Journal of Molecular and Cellular Cardiology |
Volume | 19 |
Issue number | 6 |
DOIs | |
State | Published - Jun 1987 |
Keywords
- Cardiomyopathy
- Collagen
- Fibrosis
- Scleroderma
- Tight-skin mouse
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine