Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

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

Authors: Mouw, G  Zechel, JL  Gamboa, J  Lust, WD  Selman, WR  Ratcheson, RA 
Citation: Mouw G, etal., Neuroreport 2003 Feb 10;14(2):183-6.
Pubmed: (View Article at PubMed) PMID:12598725
DOI: Full-text: DOI:10.1097/01.wnr.0000054277.81804.24

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.

Annotation

Disease Annotations
Gene Ontology Annotations
Objects Annotated

Additional Information

 
RGD Object Information
RGD ID: 1299333
Created: 2004-06-01
Species: All species
Last Modified: 2006-04-25
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.