RGD Reference Report - Two caspase-2 transcripts are expressed in rat hippocampus after global cerebral ischemia. - Rat Genome Database

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Two caspase-2 transcripts are expressed in rat hippocampus after global cerebral ischemia.

Authors: Jin, K  Nagayama, T  Mao, X  Kawaguchi, K  Hickey, RW  Greenberg, DA  Simon, RP  Graham, SH 
Citation: Jin K, etal., J Neurochem. 2002 Apr;81(1):25-35.
RGD ID: 4107080
Pubmed: PMID:12067235   (View Abstract at PubMed)

Caspase family genes play a critical role in the initiation and execution of programmed cell death. Programmed cell death is an important contributor to neuronal loss following cerebral ischemia. We have performed a series of experiments to investigate the role of a specific caspase, caspase-2, in the development of delayed neuronal death following transient global ischemia in the rat. A rat ischemic brain cDNA library was screened, and two splice-variants of caspase-2 mRNA were identified, caspase-2S and caspase-2L, which were highly homologous with the sequences of human and mouse caspase-2S and caspase-2L genes, respectively. RT-PCR demonstrated an increase in expression of both caspase-2S and caspase-2L mRNA at 8, 24 and 72 h of reperfusion after global ischemia. The ratio of the two PCR fragments did not change significantly throughout the time course of reperfusion. Western blot with monoclonal antibody specific to the pro-apoptotic caspase-2L splice variant revealed an increase in procaspase-2 (51 kDa) protein from 4 to 72 h following ischemia compared with sham-operated controls. Furthermore, an approximately 30-kDa cleavage product appeared at 8 h and increased with increasing duration of reperfusion. Thus, caspase-2L is both translated and activated following transient global ischemia. Finally, intraventricular administration of the caspase-2-like inhibitor (VDVAD-FMK) 30 min before induction of ischemia decreased the number of CA1 neurons staining positively for DNA damage (Klenow-labeling assay) and increased the number of healthy-appearing CA1 neurons (cresyl violet) compared with vehicle-treated controls. Taken together, the data suggest that caspase-2 induction and activation are important mediators of delayed neuronal death following transient global ischemia.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Stroke  ISOCasp2 (Rattus norvegicus)4107080; 4107080 RGD 
Stroke  IEP 4107080 RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of neuron apoptotic process  IMP 4107080 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Casp2  (caspase 2)

Genes (Mus musculus)
Casp2  (caspase 2)

Genes (Homo sapiens)
CASP2  (caspase 2)


Additional Information