Participation of Tenascin C in Native and Homograft Aortic Valve Degeneration

Background. Tenascin C (TnC) is a connective tissue matrix glycoprotein influencing cell proliferaton, migration and apoptosis. TnC participates in the development of pathological processes in the circulatory system including, as recently demonstrated, valvular degeneration leading to aortic valve stenosis. Homograft durability is limited by its degeneration, similar to changes appearing in cases of a typical aortic stenosis, which currently are regarded as an active remodeling process with expression of inflammatory modulators, as well as participation of cells and extracellular factors (including TnC), which under physiological conditions are involved in bone formation. Objectives. The aim of the study was a comparison of TnC expression in native stenotic aortic valves and degenerating aortic valve homografts. Material and Methods. The material included two groups of aortic valves removed during routine surgery: native stenotic valves (n = 10) and dysfunctional aortic valve homografts (n = 10). Frozen valve sections were used for immunohistochemical detection of TnC, and also for identification of cells differentiated towards myofibroblasts (SMA), macrophages (CD68) and endothelial cells (CD34, vWF). Results. TnC immunoreactivity was observed in both valve types, being significantly higher in native stenotic valves than in homografts (p = 0.007). The proportion of myofibroblasts in the total valvular cell population was insignificantly higher in native valves than in homografts. In homografts showing significantly lower total celullarity than native valves (p = 0.003), macrophages were more numerous (p = 0.005), and located mostly on the valve leaflet surfaces, while in native valves they were almost absent in this location. Conclusions. The presence of TnC in the stroma of native stenotic aortic valves and in homografts indicates a participation of active remodeling mechanisms in the pathogenesis of degeneration in both types of valves. However, a significantly lower level of TnC and lower cellularity in homografts suggests that changes leading to their dysfunction, to some extent, include passive degeneration (Adv Clin Exp Med 2011, 20, 2, 157-164).