Caspase 3 activation in nasal capillary in patients with epistaxis.

OBJECTIVE: We investigated whether an apoptosis of nasal microvessels contributes to probable mechanism of the onset of epistaxis. STUDY DESIGN AND SETTING: Nasal septal mucosa of Little's areas taken from patients without (n = 19) and with (n = 26) epistaxis were examined. Active caspase-3 in the mucosa was detected according to the methods of immunohistochemistry and Western blotting. On Western blot analysis of the homogenates of the mucosa, we also sought probable signaling factors after caspase-3 activation. RESULTS: Marked activation of caspase-3 was detected in the capillaries and its neighboring muscle cells of Little's area from patients with epistaxis, and the activation was due to enhanced expression of procaspase-3 protein and progressive cleavage of the precursor. As a result of Western blotting of signaling factors, enhanced expressions of caspase-9 and Bax protein in the homogenates of Little's area in epistaxis group were found compared with those in control group. Increased levels of cytochrome c released into a cytosol were also detected in the capillaries in epistaxis group. CONCLUSION: In the present study, caspase-3 activation was found in the capillaries of Little's area from patients with epistaxis, suggesting that an apoptosis of capillaries may contribute to a mechanism of the onset of epistaxis. Moreover, alterations of some apoptotic factors such as caspase-9, Bax, and cytochrome c in the tissues demonstrated participation of mitochondrial disturbance in one of the apoptotic mechanisms. SIGNIFICANCE: Further explorations of the pathobiologic mechanism of capillary apoptosis can lead not only to an identification of risk factors in the onset of epistaxis but also to the development of medical therapy of epistaxis.