Related Experiment Video
Updated: Aug 10, 2026

Encapsulation of Cardiomyocytes in a Fibrin Hydrogel for Cardiac Tissue Engineering
Published on: September 19, 2011
Collagen synthesis by cultured cardiac fibroblasts obtained from cardiomyopathic hamsters
T Shinohara1, M Shimizu, H Yoshio
1Second Department of Internal Medicine, School of Medicine, Kanazawa University, Japan.
Insights
Cardiomyopathic hamsters show increased collagen synthesis. The angiotensin converting enzyme inhibitor, captopril, improved collagen metabolism in these hamsters, suggesting a role for the cardiac renin-angiotensin system.
Area of Science:
- Cardiovascular Research
- Biochemistry
- Pharmacology
Background:
- Myocardial fibrosis is a hallmark of cardiomyopathy.
- Understanding collagen metabolism is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate myocardial collagen metabolism in Bio 14.6 cardiomyopathic hamsters.
- To evaluate the effects of captopril on collagen synthesis in these hamsters.
Main Methods:
- Primary cardiac fibroblast cultures from Bio 14.6 and Flb hamsters.
- Measurement of 3H-proline uptake to assess collagen synthesis.
- SDS-PAGE analysis to determine collagen types.
- Treatment with captopril (1 microM) to assess its effects.
Main Results:
- Bio 14.6 hamsters exhibited significantly higher collagenous protein synthesis compared to Flb hamsters.
- Increased synthesis of collagen types I, III, IV, and V was observed in cardiomyopathic hamsters, with type III collagen showing the greatest increase.
- Captopril treatment significantly reduced collagenous protein synthesis and qualitatively decreased type III collagen synthesis in Bio 14.6 hamsters.
Conclusions:
- Cardiac fibroblasts from Bio 14.6 hamsters display enhanced collagen synthetic activity.
- Captopril effectively improves collagen metabolism in cardiomyopathic hamster cardiac fibroblasts.
- The cardiac renin-angiotensin system may mediate captopril's beneficial effects on collagen metabolism.
Abstract:
The aim of the present study was to clarify myocardial collagen metabolism in cardiomyopathic hamsters and the effects of the angiotensin converting enzyme inhibitor, captopril, on collagen synthesis. Cardiac fibroblasts from Bio 14.6 cardiomyopathic hamsters and from non-cardiomyopathic Flb hamsters were cultured and used in the 4th passage. The synthetic activity of collagenous protein from the two types of hamsters was determined by measuring 3H-proline uptake, and the collagen type was subsequently analyzed by SDS-PAGE in cultured cardiac fibroblasts. Also studied were the effects of the angiotensin converting enzyme inhibitor captopril (1 microM) on collagen synthesis by cardiac fibroblasts from cardiomyopathic hamsters. Twenty five-week-old Bio 14.6 hamsters had significantly higher synthetic activity of collagenous protein and rate of collagen synthesis compared with 13-week-old Bio 14.6 hamsters or 25-week-old Flb hamsters [Bio 14.6(25-week); 12.4 +/- 1.6, Bio 14.6(13-week); 4.8 +/- 0.4, Flb (25-week); 8.7 +/- 0.9 cpm/cell, Bio 14.6(25-week); 11.0 +/- 0.9, Bio 14.6(13-week); 3.9 +/- 0.4, F1b (25-week); 4.8 +/- 0.4%, p < 0.05]. Qualitatively, 25-week-old Bio 14.6 hamsters had significantly higher synthetic activity of type I, III, IV and V collagens compared with 25-week-old F1b hamsters. The synthetic activity of type III collagen was increased the most in the cardiomyopathic group. Captopril (1 microM) caused a significant decrease in synthetic activity of collagenous protein in 25-week-old Bio 14.6 hamsters (12.4 +/- 1.6 cpm/cell-->10.9 +/- 1.1 cpm/cell, p < 0.05). Qualitatively, the synthetic activity of type III collagen was decreased to about half. Our study revealed enhanced collagen synthetic activity in cardiac fibroblasts from Bio 14.6 hamsters. Captopril improved collagen metabolism in cultured cardiac fibroblasts from Bio 14.6 hamsters not only quantitatively but also qualitatively. The mechanism of this improvement may be related to the cardiac renin angiotensin system.

