Related Experiment Videos
Alteration of extracellular matrix in dilated cardiomyopathic hamster heart
1Department of Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Insights
Collagen changes in dilated cardiomyopathy hearts show type III collagen increases early, while later stages feature insoluble type I collagen. This collagen remodeling may impair cardiac function.
Area of Science:
- Cardiovascular Research
- Biochemistry
- Pathology
Background:
- Dilated cardiomyopathy (DCM) involves significant structural changes in the heart.
- Collagen remodeling is implicated in the progression of cardiac diseases.
Purpose of the Study:
- To characterize collagen composition in hereditary dilated cardiomyopathic hamster hearts.
- To investigate collagen's role in DCM occurrence and progression.
Main Methods:
- Utilized BIO 53.58 hamsters as a DCM model and Flb hamsters as controls.
- Analyzed collagen content, type III collagen expression, acetic acid solubility, and reducible crosslinks at various ages (5, 10, 20 weeks).
Main Results:
- Collagen content increased with age in BIO 53.58 hamsters, unlike controls.
- Type III collagen significantly increased at 10 weeks in BIO 53.58 hamsters.
- Collagen became less soluble and shifted towards type I in later stages of DCM.
Conclusions:
- Early DCM phases are characterized by increased type III collagen in the myocardial extracellular matrix.
- Later DCM phases show a matrix resembling hard tissues, rich in insoluble type I collagen.
- Increased collagen synthesis likely impairs cardiac function during DCM development.
Abstract:
The purpose of this study was to characterize the collagen in hereditary dilated cardiomyopathic hamster hearts, and to examine the participation of the collagen in the occurrence and progression of cardiomyopathy. BIO 53.58 hamsters (5, 10, 20 weeks old) were used as the model of dilated cardiomyopathy. Flb hamsters were used as controls. The collagen content was almost constant at any age in the Flb hamsters, but increased with age in BIO 53.58 hamsters. Type III collagen increased significantly in BIO 53.58 hamsters at 10 weeks. The acetic acid solubility of collagen decreased in BIO 53.58 hamsters as the fibrosis progressed, but was unchanged in controls. Reducible crosslinks showed a tendency to decrease progressively in BIO 53.58 hamsters. There were no differences between Flb and BIO 53.58 hamsters at 5 weeks, but its expression in BIO 53.58 hamsters at 10 and 20 weeks of age increased compared to Flb controls. These findings indicate that in the early phase of cardiomyopathy the extracellular matrix of the myocardium is rich in type III collagen. In the later phase, the matrix resembles that of hard tissues, whose collagen is mainly of type I collagen and is insoluble. These data suggest that the increased collagen synthesis may impair the cardiac function in the development of cardiomyopathy.