Abstract:
:The mechanisms of injury-induced apoptosis of neurons within the spinal cord are poorly understood. In this study, we show that spinal cord injury (SCI) induces endoplasmic reticulum stress revealed by the activation of an unbalanced unfolded protein response (UPR). Using a weight-drop contusion model of SCI, the UPR activation was characterized by a quick transient phosphorylation of alpha subunit of eukaryotic initiation factor 2 soon restored by the up-regulation of its regulator Gadd34; an effective cleavage/activation of the ATF6alpha transcription factor leading to up-regulation of the canonical UPR target genes Chop, Xbp1 and Grp78; the presence of the processing of Xbp1 mRNA indicative of inositol requiring kinase 1 activation, and a gradual accumulation of C/EBP homologous transcription factor protein (CHOP) with concomitant caspase-12 activation. Interestingly, the subcellular distribution of CHOP was found in the nucleus of neurons and oligodendrocytes but in the cytoplasm of astrocytes. Considering the pro-apoptotic action attributed to this transcription factor, this phenomenon might account for the different susceptibility of cell types to dye after SCI.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Penas C,Guzmán MS,Verdú E,Forés J,Navarro X,Casas Cdoi
10.1111/j.1471-4159.2007.04671.xsubject
Has Abstractpub_date
2007-08-01 00:00:00pages
1242-55issue
4eissn
0022-3042issn
1471-4159pii
JNC4671journal_volume
102pub_type
杂志文章abstract::This Editorial highlights an ingenious study by Li and Freeman published in this issue of J. Neurochem. Accurately knowing the brain extracellular levels of the two main substrates, that is, glucose and lactate, while a well-controlled and graded-stimulus is applied, might be extremely useful to finely understand how ...
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