Distribution of myofibroblasts, smooth muscle–like cells, macrophages, and mast cells in mitral valve leaflets of dogs with myxomatous mitral valve disease

Abstract

Activated-myofibroblasts (alpha-SMA-positive cells) were increased and inactive-myofibroblasts (vimentin-positive cells) were reduced in mitral valve leaflets of dogs with MMVD, compared with that of clinically normal dogs. Impact on Human Medicine-This is the first description of spatial and temporal alterations in mitral valve cells of any species with MMVD and has clinical importance in the understanding of disease development in dogs and humans.

Pathology, protein expression and signaling in myxomatous mitral valve degeneration: Comparison of dogs and humans

“…However, evidence of direct involvement does not exist since the macrophage population mostly accumulated in the disease-free basal zone. 69 The infiltration of other inflammatory cells was not detected in diseased valves. 1,16,30 However, several inflammatory cytokine genes were up-regulated in affected canine valves.…”

“…66,67 Furthermore, an accumulation of proteoglycans, lipids and hexosamines was detected in canine MMVD. 8,68,69 Immunohistochemical studies in mild canine MMVD showed an irregularly split basement membrane. The ECM components, collagen VI and laminin were mildly increased and spread into the atrialis layer.…”

Pathology of myxomatous mitral valve disease in the dog

“…Lesions include progressive expansion of the spongiosa layer and disruption of the fibrosa layer. 4,15,17,20,24,36,78,97 Such changes can be detected most readily along the region of leaflet apposition, and early lesions may be accentuated in proximity to major chordal attachment. The spongiosa valve layer becomes thickened with increased extracellular matrix containing glycosaminoglycans (GAG, formerly described as acid mucopolysaccharides) and proteoglycans, and proliferation of edematous ground substance.…”

Correlation between systolic function and presence of myofibroblasts in doxorubicin-induced cardiomyopathy

“…In the normal myocardium, the only cells that are positive for α-SMA are vascular smooth muscle cells (PeSSANhA, et al, 1999). Recent studies in dogs, humans, and laboratory animals have demonstrated the importance of myofibroblasts distribution in injured cardiac muscle for the evolution of heart failure, and as an improvement indicator for novel therapeutic methods yet to be tested (zhANG et al, 1998;SwANeY et al, 2005;hAN, et al, 2008;ASAzuMA-NAkAMuRA et al, 2009). Accordingly, the aim of this research was to study the presence of myofibroblasts in doxorubicin-induced cardiomyopathy in rabbits through immunohistochemistry, and to correlate with Doppler echocardiography indices.…”