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Updated: Sep 21, 2026
Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
[An investigation of the collagen in cardiomyopathic hamsters]
1Hokkaido University School of Medicine, Sapporo, Japan.
Insights
Collagen changes in cardiomyopathy models show early increases in type III collagen, shifting to mature type I collagen with fibrosis progression. This impacts heart function by altering myocardial extracellular matrix composition.
Area of Science:
- Cardiovascular Biology
- Extracellular Matrix Research
- Connective Tissue Biochemistry
Context:
- Cardiomyopathy is characterized by extensive cardiac fibrosis.
- The extracellular matrix (ECM), particularly collagen, plays a crucial role in myocardial structure and function.
- Understanding collagen's role in cardiomyopathy progression is vital for therapeutic development.
Purpose:
- To characterize collagen composition and changes in hereditary cardiomyopathic hamster models.
- To examine collagen's involvement in the development and progression of dilated and hypertrophic cardiomyopathy.
- To correlate ECM alterations with functional deficits in cardiac muscle.
Summary:
- Collagen content increased with age in cardiomyopathy models (BIO53.58 and BIO14.6), unlike controls (F1b).
- Type III collagen significantly increased in early stages, while Type V collagen decreased in later stages of hypertrophic cardiomyopathy.
- Collagen solubility decreased, and thick collagen fibers increased, indicating matrix stiffening and resemblance to mature connective tissues.
Impact:
- Findings suggest early cardiomyopathy ECM resembles immature tissue, shifting to a fibrotic, mature state.
- Altered collagen structure and increased fiber thickness likely impair diastolic and systolic heart function.
- This research provides insights into ECM remodeling in heart disease, potentially guiding future therapeutic strategies.
Abstract:
Extensive fibrosis is remarkable in cardiomyopathy. The purpose of this study is to characterize the collagen, one of the chief elements of the extracellular matrix of hereditary cardiomyopathic hamsters, and to examine the participation of the collagen in the occurrence and the progression of the cardiomyopathy. BIO53.58 (5, 11, 22 weeks) was used as the model of the dilated cardiomyopathy and BIO14.6 (20, 30 weeks) was used as the model of the hypertrophic cardiomyopathy F1b was used as the control. The collagen content was almost constant at any age in F1b, but increased with aging in BIO53.58 and BIO14.6. Type III collagen increased significantly in BIO53.58 at 11 weeks and BIO14.6 at 20 weeks. Type V collagen decreased significantly in BIO14.6 at 30 weeks. Acetic acid solubility of collagen decreased in BIO53.58 and BIO14.6 with the progression of the fibrosis, but not in F1b. Reducible crosslinks showed the tendency to decrease in BIO53.58 progressively. Histologically thick collagen fiber increased in BIO53.58 and BIO14.6. These findings indicate that in the early phase of the cardiomyopathy the extracellular matrix of the myocardium has characteristics that of the immature tissues which are rich in type III collagen. In later phase, the matrix resembles that of hard tissues whose collagen is mainly of type I collagen and have low solubility. It is considered that the increase of the thick collagen fiber combined firmly in heart may affect the diastolic and the systolic function in addition to the loss of the cardiac muscle fiber by the degeneration and the necrosis.
