Decreased and inactivated nuclear factor kappa B 1 (p50) in human degenerative calcified aortic valve

BackgroundDegenerative aortic valve calcification is an important factor in aortic stenosis and incompetence, but the pathogenesis is unclear. The purpose of the present study was to observe the expression of p50 in degenerative calcified aortic valves, which may provide a potential therapeutic target.MethodsFifteen cases of degenerative calcified aortic valve constituted the experimental group, and 10 aortic valves from patients who had undergone the Bentall operation constituted the control group.ResultsImmunostaining demonstrated that α-smooth muscle actin was highly expressed in valvular interstitial cells in the experimental group and that the percentage of CD68-positive cells was significantly higher in degenerative calcified aortic valves. Using bone gamma-carboxyglutamate protein as a marker of calcification showed that osteoblasts were significantly increased in the experimental valves. Western blot showed that p50 was more highly expressed and activated in the control group compared with the experimental group. Immunohistochemistry confirmed this finding and showed that p50 was principally localized to the endothelial cells of uncalcified valves, suggesting that it might play an important role in maintaining valve function.ConclusionsInhibition of p50 activity in endothelial cells might lead to calcification in degenerative calcified aortic valves.