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

Connections (1)

This publication is referenced by other Labnodes entities:

Links