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Osteopontin expression is increased in the heritable cardiomyopathy of Syrian hamsters
E B Williams1, I Halpert, S Wickline
1Department of Internal Medicine, Washington University School of Medicine, St Louis, MO, USA.
Insights
Osteopontin is significantly upregulated in heritable cardiomyopathy in Syrian hamsters, originating from macrophage-like cells. This finding highlights osteopontin
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Immunology
Background:
- Osteopontin (a noncollagenous matrix protein) has transient cardiac expression post-injury.
- Its role in chronic cardiac remodeling, particularly in heritable cardiomyopathies, remains uncharacterized.
Purpose of the Study:
- To investigate osteopontin expression in the Syrian hamster heritable cardiomyopathy model.
- To determine the cellular source of osteopontin in the cardiomyopathic heart.
Main Methods:
- RNA isolation and analysis (quantitative PCR) of hamster hearts.
- In situ hybridization to localize osteopontin mRNA within cardiac tissue.
Main Results:
- Osteopontin mRNA levels were 12-fold higher in cardiomyopathic hamsters compared to normal controls.
- Osteopontin mRNA was localized to cells resembling tissue macrophages within foci of inflammation in cardiomyopathic hearts.
Conclusions:
- Osteopontin is expressed in heritably cardiomyopathic hamster hearts during chronic injury and repair.
- Tissue macrophage-like cells are the apparent source of osteopontin in these inflamed hearts.
- This model is suitable for studying osteopontin's role in myocardial inflammation and remodeling.
Background:
Osteopontin, a noncollagenous matrix protein, is transiently expressed in the heart after experimental cardiac injury, but its expression in states of continuing cardiac remodeling is unknown. We evaluated osteopontin expression in the heritable cardiomyopathy of the Syrian hamster.
Methods And Results:
Hamster hearts were obtained for RNA isolation and analysis and in situ hybridization from two groups: normal control animals (n = 4) and untreated cardiomyopathic hamsters (n = 5). Osteopontin mRNA was 12-fold greater in cardiomyopathic hearts compared with normal controls (1.76 +/- 0.31 versus 0.14 +/- 0.04 arbitrary units normalized to GAPDH, mean +/- SEM, P < .05). In situ hybridization was used to define the origin of osteopontin in the heart. Osteopontin mRNA above background levels was not detected in sections from noncardiomyopathic hamster hearts but was readily detected in sections from cardiomyopathic hamsters, in which it originated in cells morphologically consistent with tissue macrophages.
Conclusions:
In the hamster, osteopontin is expressed in heritably cardiomyopathic hearts under conditions of chronic injury and repair, and the source of ostopontin message appears to be issue macrophage-like cells in foci of inflammation. This model could be used to evaluate the biological role of osteopontin in myocardial inflammation and remodeling.