Neuronal apoptosis induced by endoplasmic reticulum stress

Lizhen Chen, Xiang Gao

Research output: Contribution to journalArticlepeer-review

37 Scopus citations

Abstract

Apoptosis is a conserved active cellular mechanism occurring under a range of physiological and pathological conditions. In the nervous system, apoptosis plays crucial roles in normal development and neuronal degenerating diseases. Various deleterious conditions, including accumulation of the mutant proteins in the endoplasmic reticulum (ER) and inhibition of ER to Golgi transport of proteins, may result in apoptosis. In this study, we examined the downstream events of apoptosis in differentiated PC 12 cells under ER stress induced by brefeldin A, an inhibitor of ER to Golgi protein transport. Activation of NF-κB and degradation of I-κB were observed within 2 hours, followed by up-regulation of GRP78 protein level in treated cells. Caspase-12 only appeared around 24 hours after brefeldin A treatment, coincident with cell nuclei fragmentation. These results suggest that neuronal apoptosis may be induced by ER stress through a NF-κB and caspase related pathway.

Original languageEnglish (US)
Pages (from-to)891-898
Number of pages8
JournalNeurochemical Research
Volume27
Issue number9
DOIs
StatePublished - Sep 1 2002
Externally publishedYes

Keywords

  • Apoptosis
  • Caspase
  • ER stress
  • GRP78
  • NF-κB

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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