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- W4231579694 abstract "The signalling pathways mediating neutrophil spontaneous apoptosis are still largely unknown. We report that the indolocarbazole compound KT5823, a specific inhibitor of cGMP-dependent protein kinases (cGK), dose-dependently inhibited spontaneous apoptosis of neutrophils. At the concentration eliciting the maximum effect (8 μM), it decreased apoptosis from 72.42 ± 12.79% to 45.86 ± 7.22% (p=0.0002, n=6). Similarly, the isoquinoline sulfonamide compound H89, another cGK inhibitor, prevented neutrophil apoptosis. At the concentration eliciting the maximum effect (20 μM), it decreased apoptosis from 72.42 ± 12.79% to 31.84 ± 10.70% (p=0.0004, n=6). The maximum effect of KT5823 and H89 was comparable to that of GM-CSF and LPS, respectively. Moreover, YC-1, a soluble guanylate cyclase activator, and 4-{[3′,4′,-(methylenedioxy)benzyl]amino}-6-methoxyquinazoline, a specific phosphodiesterase 5 inhibitor, enhanced neutrophil apoptosis, and their effect was antagonised by KT5823. Taken together, these observations highlight a new role of cGK as important mediators of neutrophil spontaneous apoptosis." @default.
- W4231579694 created "2022-05-12" @default.
- W4231579694 date "2003-01-01" @default.
- W4231579694 modified "2023-09-24" @default.
- W4231579694 title "Author Index" @default.
- W4231579694 doi "https://doi.org/10.1016/s0006-291x(03)00006-8" @default.
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