pneumoniae down stream and or upstream of cytochrome c release, c

pneumoniae down stream and or upstream of cytochrome c release, consist ent with inhibition of apoptosis at license with Pfizer several levels of the apoptotic mitochondrial pathway. One report indicated that apoptosis of endothelial cells was indeed inhibited by infection with C. pneumoniae, although cell death by necrosis was not. Necrosis of these cells was correlated to an increased concentration of Discussion The current in vitro neuronal studies demonstrate that infection of human neuroblastoma cells by C. pneumo niae has an effect on apoptosis following staurosporine induction, as measured by characteristics of apoptosis such as nuclear fragmentation, cytoplasmic membrane inversion, and caspase 3 7 activation. The data suggest that neuronal cells can develop and maintain a chronic and prolonged infection with C.

pneumoniae through 10 days post infection. Inhibition of apoptosis was measured from 24 hours through 10 days post infection, and apop tosis inhibition was observed throughout this period. However, C. pneumoniae had a more robust effect on inhibiting apoptosis in neuronal cells at 24 hr post infec tion as compared Inhibitors,Modulators,Libraries to 10 day post infection. These results are consistent with other studies that have determined that C. pneumoniae infection inhibits Inhibitors,Modulators,Libraries apoptosis in mono cytes, neutrophils, and epithelial cells. Human neuroblastoma cell lines can be induced to undergo apoptosis when incubated in staurosporine at several concentrations. Staurosporine is a potent inhibitor of numerous kinases, including protein kinase C and cAMP dependent protein kinases, calmodulin dependent protein kinase, and receptor tyrosine kinases.

In cells undergoing staurosporine induced intracellular reactive oxygen species following infection. Interestingly, while there is evidence for the induction of apoptosis in the Alzheimers diseased brain, data on the completion of this Inhibitors,Modulators,Libraries process are questionable. In AD brains, increased levels of pro apoptotic proteins govern ing mitochondrial integrity and caspase activity have been demonstrated. These data suggest that caspase activation may be a key factor in modulating the apoptotic process in neurons. In vitro experiments have shown that amyloid peptides can activate the caspase cascade in neu rons resulting in cell death. However, the extent to which neurons die in AD as a result of apoptosis remains controversial.

Apoptosis is not necessarily congruent with a slow, pro gressive neurodegenerative disease. It is plausible that neuronal cell death may occur through several mecha nisms even though neurodegeneration may commence Inhibitors,Modulators,Libraries along with early apoptotic events. At first glance, our infection data appear to controvert Inhibitors,Modulators,Libraries findings of significant neuronal degeneration and cell death. However, because infection with C. pneumoniae can both inhibit selleck kinase inhibitor apoptosis and promote cell death by necrosis, and because we have continually observed C.

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