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The Journal of Neuroscience, December 15, 2001, 21(24):9519-9528
Caspase-9 Activation Results in Downstream Caspase-8 Activation and Bid Cleavage in 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinson's Disease
Veena Viswanath2, Yongqin Wu1, Rapee Boonplueang1, 2, Sylvia Chen1, Fang Feng Stevenson1, Ferda Yantiri2, Lichuan Yang3, M. Flint Beal3, and Julie K. Andersen1, 2 1 Buck Institute for Age Research, Novato, California 94945, 2 Division of Neurogerontology, Andrus Gerontology Center and Program in Molecular Biology, Department of Biological Sciences, University of Southern California, Los Angeles, California 90089, and 3 Department of Neurology, Cornell University Medical College, New York, New York 10021
Parkinson's disease (PD) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity are both associated with dopaminergic neuron death in the substantia nigra (SN). Apoptosis has been implicated in this cell loss; however, whether or not it is a major component of disease pathology remains controversial. Caspases are a major class of proteases involved in the apoptotic process. To evaluate the role of caspases in PD, we analyzed caspase activation in MPTP-treated mice, in cultured dopaminergic cells, and in postmortem PD brain tissue. MPTP was found to elicit not only the activation of the effector caspase-3 but also the initiators caspase-8 and caspase-9, mitochondrial cytochrome c release, and Bid cleavage in the SN of wild-type mice. These changes were attenuated in transgenic mice neuronally expressing the general caspase inhibitor protein baculoviral p35. These mice also displayed increased resistance to the cytotoxic effects of the drug. MPTP-associated toxicity in culture was found temporally to involve cytochrome c release, activation of caspase-9, caspase-3, and caspase-8, and Bid cleavage. Caspase-9 inhibition prevented the activation of both caspase-3 and caspase-8 and also inhibited Bid cleavage, but not cytochrome c release. Activated caspase-8 and caspase-9 were immunologically detectable within MPP+-treated mesencephalic dopaminergic neurons, dopaminergic nigral neurons from MPTP-treated mice, and autopsied Parkinsonian tissue from late-onset sporadic cases of the disease. These data demonstrate that MPTP-mediated activation of caspase-9 via cytochrome c release results in the activation of caspase-8 and Bid cleavage, which we speculate may be involved in the amplification of caspase-mediated dopaminergic cell death. These data suggest that caspase inhibitors constitute a plausible therapeutic for PD.
Key words: caspases; substantia nigra; Parkinson's disease; MPTP; mesencephalic cultures; PC12
Copyright © 2001 Society for Neuroscience 0270-6474/01/21249519-10$05.00/0
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