Hypoxic neuronal necrosis: protein synthesis-independent activation of a cell death program
J Niquet, RA Baldwin, SG Allen… - Proceedings of the …, 2003 - National Acad Sciences
J Niquet, RA Baldwin, SG Allen, DG Fujikawa, CG Wasterlain
Proceedings of the National Academy of Sciences, 2003•National Acad SciencesHypoxic necrosis of dentate gyrus neurons in primary culture required the activation of an
orderly cell death program independent of protein synthesis. Early mitochondrial swelling
and loss of the mitochondrial membrane potential were accompanied by release of
cytochrome c and followed by caspase-9-dependent activation of caspase-3. Caspase-3
and-9 inhibitors reduced neuronal necrosis. Calcium directly induced cytochrome c release
from isolated mitochondria. Hypoxic neuronal necrosis may be an active process in which …
orderly cell death program independent of protein synthesis. Early mitochondrial swelling
and loss of the mitochondrial membrane potential were accompanied by release of
cytochrome c and followed by caspase-9-dependent activation of caspase-3. Caspase-3
and-9 inhibitors reduced neuronal necrosis. Calcium directly induced cytochrome c release
from isolated mitochondria. Hypoxic neuronal necrosis may be an active process in which …
Hypoxic necrosis of dentate gyrus neurons in primary culture required the activation of an orderly cell death program independent of protein synthesis. Early mitochondrial swelling and loss of the mitochondrial membrane potential were accompanied by release of cytochrome c and followed by caspase-9-dependent activation of caspase-3. Caspase-3 and -9 inhibitors reduced neuronal necrosis. Calcium directly induced cytochrome c release from isolated mitochondria. Hypoxic neuronal necrosis may be an active process in which the direct effect of hypoxia on mitochondria may lead to the final common pathway of caspase-3-mediated neuronal death.
National Acad Sciences