Soluble Vascular Cell Adhesion Molecule-1 (VCAM-1) as a Biomarker in the Mouse Model of Experimental Autoimmune Myocarditis (EAM).
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Grabmaier U
Medical Department I, Ludwig-Maximilians-University, Munich, Germany.
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Kania G
Research of Systemic Autoimmune Diseases, Division of Rheumatology, University Hospital of Zurich, Zurich, Switzerland.
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Kreiner J
Medical Department I, Ludwig-Maximilians-University, Munich, Germany.
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Grabmeier J
Medical Department I, Ludwig-Maximilians-University, Munich, Germany.
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Uhl A
Medical Department I, Ludwig-Maximilians-University, Munich, Germany.
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Huber BC
Medical Department I, Ludwig-Maximilians-University, Munich, Germany.
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Lackermair K
Medical Department I, Ludwig-Maximilians-University, Munich, Germany.
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Herbach N
Institute of Veterinary Pathology, Ludwig-Maximilians-University, Munich, Germany.
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Todica A
Department of Nuclear Medicine, Ludwig-Maximilians-University, Munich, Germany.
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Eriksson U
Cardioimmunology, Center of Molecular Cardiology, University of Zurich, Zurich, Switzerland.
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Weckbach LT
Medical Department I, Ludwig-Maximilians-University, Munich, Germany.
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Brunner S
Medical Department I, Ludwig-Maximilians-University, Munich, Germany.
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English
Vascular cell adhesion molecule-1 (VCAM-1) is strongly upregulated in hearts of mice with coxsackie virus-induced as well as in patients with viral infection-triggered dilated cardiomyopathy. Nevertheless, the role of its soluble form as a biomarker in inflammatory heart diseases remains unclear. Therefore, we investigated whether plasma levels of soluble VCAM-1 (sVCAM-1) directly correlated with disease activity and progression of cardiac dysfunction in the mouse model of experimental autoimmune myocarditis (EAM). EAM was induced by immunization of BALB/c mice with heart-specific myosin-alpha heavy chain peptide together with complete Freund`s adjuvant. ELISA revealed strong expression of cardiac VCAM-1 (cVCAM-1) throughout the course of EAM in immunized mice compared to control animals. Furthermore, sVCAM-1 was elevated in the plasma of immunized compared to control mice at acute and chronic stages of the disease. sVCAM-1 did not correlate with the degree of acute cardiac inflammation analyzed by histology or cardiac cytokine expression investigated by ELISA. Nevertheless, heart to body weight ratio correlated significantly with sVCAM-1 at chronic stages of EAM. Cardiac systolic dysfunction studied with positron emission tomography indicated a weak relationship with sVCAM-1 at the chronic stage of the disease. Our data provide evidence that plasma levels of sVCAM-1 are elevated throughout all stages of the disease but showed no strong correlation with the severity of EAM.
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Language
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Open access status
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gold
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Persistent URL
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https://sonar.ch/global/documents/96978
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