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- W1534996904 abstract "Abstract This study investigates the implication of mitochondria‐ and caspase‐dependent pathways in the death of retinal neurones exposed to the neurosteroid pregnenolone sulfate (PS) shown to evoke apoptosis and contribute to amplification and propagation of excitotoxicity. After a brief PS challenge of intact retinas, caspase‐3 and caspase‐2 activation and cytochrome c release occur early and independent of changes in the oxidative state measured by superoxide dismutase activity. The temporal and spatial relationship of these events suggests that a caspase‐3‐dependent pathway is activated in response to cytochrome c release and requires caspase‐2 activation and a late cytochrome c release in specific cellular subsets of retinal layers. The protection by caspase inhibitors indicates a predominant role of the pathway in PS‐induced retinal apoptosis, although a limited use of caspase inhibitors is upheld on a conceivable shift from apoptosis toward necrosis. Conversely, 3α‐hydroxy‐5β‐pregnan‐20‐one sulfate and 17β‐oestradiol provide complete prevention of PS‐induced retinal death." @default.
- W1534996904 created "2016-06-24" @default.
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- W1534996904 date "2002-12-01" @default.
- W1534996904 modified "2023-10-18" @default.
- W1534996904 title "A caspase-3-dependent pathway is predominantly activated by the excitotoxin pregnenolone sulfate and requires early and late cytochrome c release and cell-specific caspase-2 activation in the retinal cell death" @default.
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- W1534996904 doi "https://doi.org/10.1046/j.1471-4159.2002.01229.x" @default.
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