Activation of caspase-12, an endoplasmic reticulum resident caspase, after permanent focal ischemia in rat.

Mouw G, Zechel JL, Gamboa J, Lust WD, Selman WR, Ratcheson RA
Neuroreport. 2003 14 (2): 183-6

PMID: 12598725 · DOI:10.1097/00001756-200302100-00004

The endoplasmic reticulum (ER) is emerging as a contributory component of cell death after ischemia. Since caspase-12 has been localized to the ER and is a novel signal for apoptosis, we examined the message levels and protein expression of caspase-12 after cerebral ischemia in vivo. Animals underwent permanent middle cerebral artery occlusion (MCAO) and were sacrificed 24 h after ischemia. Protein analysis revealed a significant increase in caspase-12 and a corresponding up-regulation of caspase-12 mRNA in the ischemia group compared with that in the sham group. Immunohistochemical analysis revealed diffuse positive immunostaining of caspase-12 throughout the striatum and cerebral cortex in animals that underwent ischemia, with more intense caspase-12 immunostaining in the striatum than in the cortex after ischemia. These results demonstrate that cerebral ischemia initiates an ER-based stress response that results in the transcriptional up-regulation and corresponding increased expression of caspase-12 protein, and may provide a new area for therapeutic intervention to ameliorate outcomes following stroke.

MeSH Terms (9)

Animals Brain Ischemia Caspase 12 Caspases Endoplasmic Reticulum Enzyme Activation Male Rats Rats, Wistar

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