Galectin-3 in cardiac muscle and circulation of dogs with degenerative mitral valve disease

ObjectivesThis study aimed to determine the association of cardiac fibrosis with the galectin-3 (Gal-3) expression, a fibrosis marker in the myocardium and to compare plasma Gal-3 levels in normal and degenerative mitral valve disease (DMVD) dogs.AnimalsStudies of muscle expression and plasma levels of Gal-3 were performed in separate groups of dogs. The tissue study was performed on cardiac tissues collected from 22 dogs. The plasma study was performed on 46 client-owned dogs.MethodsPapillary muscle and left ventricular (LV) wall obtained from 10 normal and 12 DMVD dogs were stained with Masson trichrome and Gal-3 immunohistochemistry to determine fibrosis areas and Gal-3 expression. Plasma samples were collected from 19 normal and 27 DMVD dogs for Gal-3 measurement by ELISA.ResultsPercentage of fibrosis was higher in papillary muscle and LV wall of DMVD dogs (66.13 ± 5.58%; 52.98 ± 8.45%) than in normal dogs (35.40 ± 8.46%; 27.41 ± 7.91%; p < 0.0001). Gal-3 was higher in papillary muscle and LV wall of DMVD dogs (27.95 ± 6.94%; 17.25 ± 8.76%) than in normal dogs (1.08 ± 0.67%; 0.52 ± 0.42%; p < 0.0001). Fibrosis areas correlated strongly with the Gal-3 expression (r = 0.821, p < 0.0001). Plasma Gal-3 levels were increased in DMVD dogs (1.50; 0.87–2.36 ng/mL) compared to normal dogs (0.42; 0.27–0.63 ng/mL; p < 0.0001).ConclusionsGal-3 expression in cardiac muscle was associated with cardiac fibrosis and was higher in DMVD dogs than in normal dogs. DMVD dogs had higher plasma Gal-3 concentrations than normal dogs. Tissue Gal-3 is a candidate of fibrosis biomarker in DMVD; however, further investigation of associations between plasma Gal-3 and myocardial fibrosis is necessary.