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J Biol Chem, Vol. 274, Issue 22, 15725-15731, May 28, 1999
§,,,
From the Departments of Activated microglia have been implicated in the
regulation of neuronal cell death. However, the biochemical mechanism
for neuronal death triggered by activated microglia is still unclear. When treated with activated microglia, neuronal PC12 cells undergo apoptosis accompanied by caspase-3-like protease activation and DNA
fragmentation. Apoptotic bodies formed were subsequently phagocytosed by neighboring activated microglia. Pretreatment of the cells with the
caspase-3-like protease inhibitor
N-acetyl-Asp-Glu-Val-Asp-aldehyde did not reverse this cell
death. Although Bcl-2 overexpression in the cells caused the inhibition
of caspase-3-like protease activity and DNA fragmentation and the
effective interference of apoptosis induced by deprivation of trophic
factors, it could not suppress the activated microglia-induced neuronal
death. At the electron microscopic level, degenerating cells with high
levels of Bcl-2 were characterized by slightly condensed chromatins
forming irregular-shaped masses, severely disintegrated perikarya, and marked vacuolation. Various protease inhibitors tested did not inhibit
this cell death, whereas the radical oxygen species scavenger N-acetyl-L-cysteine significantly suppressed
this death. Altogether, our study provides an alternative death pathway
for the activated microglia-induced neuronal death by blockage of the
caspase-3 protease cascade.
Pharmacology and
§ Conservative Dentistry II, Faculty of Dentistry, Kyushu
University, Fukuoka 812-8582, Japan and ¶ Tsukuba Research
Laboratories, Nippon Glaxo Ltd., Tsukuba 300-4247, Japan
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