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P38 MAP KINASE AND CASPASE - 3 MEDIATE Fe2+ - INDUCED NEURONAL DEATH IN CORTICAL CELL CULTURES


, : P38 MAP KINASE AND CASPASE - 3 MEDIATE Fe2+ - INDUCED NEURONAL DEATH IN CORTICAL CELL CULTURES. Society for Neuroscience Abstract Viewer & Itinerary Planner : Abstract No 292 17

We examined the possibility that p38 MAP kinase and CASPASE-3, the main mediators of cell death, would mediate free radical-induced neuronal cell NECROSIS. As previously reported, cortical cell cultures exposed to 30 uM Fe2+ underwent widespread neuronal cell necrosis evident by marked cell body swelling over the next 24 hr. The active form of p38 MAP kinase was observed within 4 hr following exposure of cortical cultures to Fe2+. Inclusion of PD169316, a selective inhibitor of p38 MAP kinase, attenuated Fe2+-induced neuronal cell necrosis. We next examined if CASPASE-3 would also mediate Fe2+ neurotoxocity as a downstream signal of p38 MAP kinase. The active fragment of CASPASE-3 was observed within 12 hr following exposure of cortical cell cultures to Fe2+. Fe2+-induced neuronal death was attenuated by inclusion of z-VAD-fmk,a broad-spectrum inhibitor of caspases. However, inclusion of PD169316 did not block Fe2+-induced activation of CASPASE-3, suggesting that p38 MAP kinase and CASPASE-3 separately mediate Fe2+-induced free radical neurotoxicity. In support of this, concurrent administration of PD169316 and z-VAD-fmk synergistically prevented Fe2+ neurotoxicity. The present study suggests that the well-known mediators of APOPTOSIS , p38 MAP kinase and CASPASE-3 also mediate Fe2+-induced neuronal cell necrosis possibly through separate routes.

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