Programmed cell death (Apoptosis) and its role in the pathogenesis of XXXX .

@entity6312 @entity1 @entity4910 @entity588
The etiology of @entity6312 remains elusive. We hypothesized that abnormal cell cycle events in the vein wall may contribute to changes in its structural integrity predisposing to varicosity development. Since cell cycle checkpoint controls are linked to the signaling and execution of apoptotic cascades, possibly apoptosis is a contributing factor in the pathophysiology of varicosities. The present study was designed to investigate whether programmed cell death varies in varicosities as compared to normal veins. Twenty-seven normal greater saphenous vein specimens were obtained from @entity1 undergoing infrainguinal arterial bypass surgery, and 20 varicose vein specimens were retrieved from @entity1 undergoing varicose vein excision. Apoptosis was detected by TUNEL assay. Expression of @entity588 and @entity4910 was noted by standard immunohistochemical techniques. Apoptotic cells were identified in 32 of the 47 specimens. Forty-eight percent of normal vein specimens displayed >3 apoptotic cells per 100 cells in the adventitia; 15% of the specimens of the varicose vein group showed such magnitude of apoptosis (p < 0.03). This increased apoptotic activity was not observed in media or intima of either vein group (p < 0.001). No significant difference in immunoreactivity to @entity588 protein was observed in varicose vein specimens as compared to controls. Varicose vein specimens demonstrated increased nuclear expression of @entity4910 whereas its cytoplasmic expression was significantly diminished (p </=0.02). These data show that programmed cell death is inhibited in @entity6312 . Differential expression of @entity4910 suggests that it may deregulate cell cycle events, thereby leading to varicosity formation.
