Galectin-3 as a Fibrosis Marker in Dogs with Degenerative Mitral Valve Disease
Cardiac fibrosis is a pathological change in human and canine cardiovascular disease. Galectin-3 (Gal-3), a marker of cardiac fibrosis, is upregulated in heart disease patients. A use of Gal-3 to detect cardiac fibrosis in degenerative mitral valve disease (DMVD) dogs has not been studied.
The aims of this study were to determine the expression of Gal-3 in cardiac muscles and measure level of plasma Gal-3 in CHF dogs with DMVD.
Control (n = 10) and DMVD (n = 12) cardiac samples from necropsy dogs with age > 6 years and weight < 15 kg were stained with Masson trichrome and Gal-3 immunohistochemistry. Gal-3 concentration was measured in plasma samples from control (n = 19) and DMVD (n = 27) dogs by ELISA test kits.
Fibrosis area was higher in DMVD than normal dogs (p < 0.01), apparently in subendocardium and papillary muscles (Figure 1). Gal-3 was overexpressed in DMVD than normal dogs (p < 0.01), particularly in subendocardium (Figure 2). Plasma Gal-3 concentration was significantly increased in DMVD (1.498; 0.874–2.360 ng/ml) compared to normal dogs (0.420; 0.271–0.630 ng/ml) (p < 0.01).
|Figure 1. Subendocardial fibrosis in normal (A) and DMVD dogs (B)|
Masson trichrome stain, 20x magnification
|Figure 2. Gal-3 expression in papillary (A, B) and LV (C, D) of normal and DMVD dogs, respectively|
LSAB, IHC, Mayer's hematoxylin, 20x magnification
Gal-3 expression is associated with cardiac fibrosis. Gal-3 could be a potential candidate marker of cardiac fibrosis in DMVD dogs.