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Apoptotic mitochondrial pathway in neuron and astrocyte after neonatal hypoxia-ischemia in the rat brain.

Abstract : Neuronal apoptosis plays an essential role in early brain development and contributes to secondary neuronal loss after acute ischaemia. Recent studies have provided evidence that caspase-3 is an important downstream event after hypoxia-ischaemia in the immature brain, but a minor event in the adult brain. Our investigations have focused on cell populations that expressed apoptotic effectors in the enzymatic death pathway including cytochrome c, caspase-9 and caspase-3. Expression, activation and cellular localization of these proteins were studied using cleavage of fluorogenic substrate and immunohistochemistry in neonatal rat brain after unilateral focal ischaemia. Caspase-3 enzyme activity was elevated in brain homogenate between 6 and 48 h after reperfusion. This activation was preceded by that of caspase-9, between 3 and 24 h. Apoptotic cell death was finally accomplished by poly-ADP-ribose polymerase cleavage, an endogenous caspase-3 substrate. In addition, immunodetection demonstrated that cytochrome c and activated caspase-9 and caspase-3 were expressed not only in the neurones, the primarily affected cells, but also within the astrocytes, which constituted a dense network delineating the infarct. These results suggested that glial injury may promote the formation of cystic lesions such as those observed clinically in the newborn brain.
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https://hal.archives-ouvertes.fr/hal-00078502
Contributor : Therese Ghembaza <>
Submitted on : Tuesday, June 6, 2006 - 2:40:05 PM
Last modification on : Monday, August 31, 2020 - 11:42:26 AM

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N. Benjelloun, L. M. Joly, B. Palmier, M. Plotkine, C. Charriaut-Marlangue. Apoptotic mitochondrial pathway in neuron and astrocyte after neonatal hypoxia-ischemia in the rat brain.. Neuropathol. and Applied Neurobiol., 2003, 29, pp.350-360. ⟨10.1046/j.1365-2990.2003.00467.x⟩. ⟨hal-00078502⟩

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