Matrix Gla protein regulates XXXX of the aortic valve.

@entity1 @entity9198 @entity730 @entity729 @entity472
BACKGROUND: The aortic valve interstitial cell (AVIC) has been implicated in the pathogenesis of @entity472 . In response to proinflammatory stimulation, the AVIC undergoes a phenotypic change from that of a myofibroblast phenotype to that of osteoblast-like cell. @entity9198 ( @entity9198 ) has been identified as an important inhibitor of @entity729 . We therefore hypothesized that @entity9198 expression is reduced in diseased AVICs, and loss of this protective protein contributes to @entity730 of the aortic valve. Our purpose was to compare @entity9198 expression in normal versus diseased AVICs. MATERIALS AND METHODS: @entity1 AVICs were isolated from normal aortic valves from explanted hearts (n  =  6) at the time of heart transplantation. AVICs were also isolated from calcified, diseased valves of @entity1 (n  =  6) undergoing aortic valve replacement. AVICs were grown in culture until they reached passages 2-6 before experimentation. Immunofluorescent staining, reverse transcriptase-polymerase chain reaction, immunoblotting, and enzyme-linked immunosorbent assay were used to compare levels of @entity9198 in normal and diseased AVICs. Statistics were performed using the Mann-Whitney U test (P  <  0.05). RESULTS: @entity9198 expression was significantly decreased in diseased AVICs relative to normal AVICs by immunofluorescent staining, reverse transcriptase-polymerase chain reaction, immunoblotting, and enzyme-linked immunosorbent assay. CONCLUSIONS: An important anti- @entity730 defense mechanism is deficient in calcified aortic valves. @entity9198 expression is significantly lower in diseased relative to normal AVICs. Lack of this important "anti- @entity730 " protein may contribute to @entity730 of the aortic valve.
