EXPRESSION OF GALECTIN-3 IN CARDIAC MUSCLES AND DETERMINATION LEVEL OF PLASMA GALECTIN-3 IN DOGS WITH DEGENERATIVE MITRAL VALVE DISEASE

Abstract

Degenerative mitral valve disease (DMVD) is a common acquired cardiac disease in older small breed dogs. The pathophysiology of this disease is similar to mitral valve prolapse (MVP) in humans. MVP and other cardiovascular diseases in human can cause cardiac fibrosis. DMVD dogs also have cardiac fibrosis like human. Gal-3, has been used as a cardiac fibrosis marker in humans. Gal-3 is up-regulated in cardiac muscles and blood circulation of CHF patients. A role of Gal-3 as a cardiac fibrosis marker in dogs with naturally occurring DMVD has not been studied. The aims of this study were to determine expression of Gal-3 in cardiac muscles and measure level of plasma Gal-3 in DMVD dogs. Twelve DMVD and ten normal cardiac muscles from small breed less than 15 kilograms and older than 6 years old necropsy dogs were collected to determine cardiac fibrosis and Gal-3 expression by Masson trichrome and Gal-3 immunohistochemistry staining, respectively. Plasma Gal-3 concentration was measured from 19 normal and 27 aged, sized and breed matched DMVD dogs by ELISA test kits. Age and weight were not correlated with cardiac fibrosis and Gal-3 expression. DMVD dogs had more cardiac fibrosis (p < 0.01) and overexpressed of Gal-3 (p < 0.01) than normal dogs particularly in sub-endocardium. Plasma Gal-3 concentration was significantly higher in DMVD than normal dogs (p < 0.01). Age, weight and echocardiographic indices showed no correlation with plasma Gal-3 concentration. In conclusion, Gal-3 might be a potential candidate of cardiac fibrosis markers in dogs with DMVD.