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Published on: January 28, 2020
Osteopontin: a biomarker to predict the outcome of inflammatory heart disease
Karin Klingel1, Reinhard Kandolf
1Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany. karin.klingel@med.uni-tuebingen.de
Insights
Osteopontin (OPN) is crucial in heart inflammation and fibrosis. Elevated OPN in macrophages signals active cardiac inflammation, potentially serving as a biomarker for myocarditis before heart damage occurs.
Area of Science:
- Cardiology
- Immunology
- Pathology
Background:
- Virus-induced myocarditis can lead to chronic inflammation, disrupting the heart's matrix and causing dysfunction.
- Cardiomyocyte death triggers immune responses involving macrophages and T cells, with cytokines like IL-10 and TGF-β regulating inflammation.
- Osteopontin (OPN), a matricellular protein, plays a role in inflammatory pathways and cardiac repair.
Purpose of the Study:
- To investigate the role of osteopontin (OPN) in viral myocarditis, specifically its impact on fibrosis and cardiac remodeling.
- To determine if OPN expression in macrophages can serve as a biomarker for active cardiac inflammation.
Main Methods:
- Utilized a coxsackievirus B3-induced myocarditis mouse model.
- Analyzed OPN expression in macrophages in both the animal model and human patient samples (acute/chronic myocarditis, dilated cardiomyopathy).
Main Results:
- Early OPN expression in macrophages was identified as a key factor in fibrosis and cardiac remodeling in the model.
- OPN did not affect the antiviral immune response efficacy.
- High OPN expression in macrophages was observed in patients with acute and chronic myocarditis, but not in end-stage dilated cardiomyopathy.
Conclusions:
- Cardiac OPN expression, particularly in macrophages, is linked to ongoing inflammation in myocarditis.
- OPN may serve as a valuable biomarker for detecting cardiac inflammation preceding fibrosis and adverse cardiac remodeling.
Abstract:
Inflammatory processes of the heart are often induced by viruses. Although most acute virus-induced myocarditis quickly resolves, some patients develop chronic myocarditis resulting in a considerable disruption of the myocardial matrix network, finally leading to cardiac dysfunction. The death of cardiomyocytes due to virus replication is followed by the attraction of macrophages and T cells to the sites of cardiac damage. Ongoing inflammation is usually suppressed by interleukin-10 and transforming growth factor-beta production, thus activating myofibroblasts and secretion of extracellular matrix proteins like collagen type I. Also, osteopontin (OPN), a matricellular protein with cytokine-like properties, is critically involved in inflammatory pathways and can modulate the cell biology of cardiac repair. In our model of coxsackievirus B3-induced myocarditis, we have shown that increased early OPN expression in macrophages is a determinant of fibrosis and enhanced cardiac remodeling. OPN was not found to influence the efficacy of the antiviral immune response. Also, in patients with acute and chronic myocarditis, but not in patients with end-stage dilated cardiomyopathy, we found a high OPN expression in macrophages, indicating active inflammatory processes. Thus cardiac OPN expression might be considered as a biomarker indicating ongoing cardiac inflammation preceding fibrosis and remodeling of the heart.
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