Journal
NEUROBIOLOGY OF DISEASE
Volume 29, Issue 2, Pages 221-231Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2007.08.015
Keywords
Golgi fragmentation; ER stress; apoptosis; mitochondria; Alzheimer's disease; amyotrophic lateral sclerosis; excitotoxicity; NMDA; oxidative stress; nitrosative stress
Categories
Funding
- NEI NIH HHS [R01 EY005477-23, R01 EY09024, R01 EY016164, R01 EY005477, R01 EY009024-18, R01 EY05477, R01 EY009024] Funding Source: Medline
- NICHD NIH HHS [P01 HD029587, P01 HD29587, P01 HD029587-14] Funding Source: Medline
- NIGMS NIH HHS [R01 GM56737, R01 GM046224, R01 GM46224] Funding Source: Medline
- NINDS NIH HHS [R01 NS043242, P30 NS057096, R01 NS044326, R01 NS044326-05, R01 NS043242-04] Funding Source: Medline
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The Golgi apparatus processes intracellular proteins, but undergoes disassembly and fragmentation during apoptosis in several neurodegenerative disorders such as amyotrophic lateral sclerosis and Alzheimer's disease. It is well known that other cytoplasmic organelles play important roles in cell death pathways. Thus, we hypothesized that Golgi fragmentation might participate in transduction of cell death signals. Here, we found that Golgi fragmentation and dispersal precede neuronal cell death triggered by excitotoxins, oxidative/nitrosative insults, or ER stress. Pharmacological intervention or overexpression of the C-terminal fragment of Grasp65, a Golgi-associated protein, inhibits fragmentation and decreases or delays neuronal cell death. Inhibition of mitochondrial or ER cell death pathways also decreases Golgi fragmentation, indicating crosstalk between organelles and suggesting that the Golgi may be a common downstream-effector of cell death. Taken together, these findings implicate the Golgi as a sensor of stress signals in cell death pathways. (C) 2007 Elsevier Inc. All rights reserved.
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