Journal
NEUROBIOLOGY OF DISEASE
Volume 36, Issue 3, Pages 470-476Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2009.08.013
Keywords
Amyotrophic lateral sclerosis (ALS); Astrocyte; C/EBP homologous protein (CHOP); Endoplasmic reticulum (ER) stress; Superoxide dismutase 1 (SOD1); Spinal cord
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Funding
- Japan Society for the Promotion of Science [20-10786]
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Endoplasmic reticulum (ER) stress-induced neuronal death may play a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS). However, whether CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP), an ER-stress apoptotic mediator, is involved in the pathogenesis of ALS is controversial. Here we demonstrate the expression levels and localization of CHOP in spinal cords of both sporadic ALS patients and ALS transgenic mice by immunohistochemistry. In the spinal cords of sporadic ALS patients, CHOP was markedly up-regulated but typically expressed at low levels in those of the control. Likewise, CHOP expression increased at 14 (symptomatic stage) and 18 to 20 weeks (end stage) in ALS transgenic mice spinal cords. Furthermore, localizations of CHOP were merged in motor neurons and glial cells, such as oligodendrocytes, astrocytes, and microglia. These results indicate that the up-regulation of CHOP in motor neurons and glial cells may play pivotal roles in the pathogenesis of ALS. (C) 2009 Elsevier Inc. All rights reserved.
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