RGD Reference Report - Gene expression analysis of spontaneously hypertensive rat cerebral cortex following transient focal cerebral ischemia. - Rat Genome Database

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Gene expression analysis of spontaneously hypertensive rat cerebral cortex following transient focal cerebral ischemia.

Authors: Raghavendra Rao, VL  Bowen, KK  Dhodda, VK  Song, G  Franklin, JL  Gavva, NR  Dempsey, RJ 
Citation: Raghavendra Rao VL, etal., J Neurochem 2002 Dec;83(5):1072-86.
RGD ID: 632385
Pubmed: PMID:12437578   (View Abstract at PubMed)

Identification of novel modulators of ischemic neuronal death helps in developing new strategies to prevent the stroke-induced neurological dysfunction. Hence, the present study evaluated the gene expression changes in rat cerebral cortex at 6 and 24 h of reperfusion following transient middle cerebral artery occlusion (MCAO) by GeneChip analysis. Transient MCAO resulted in selective increased mRNA levels of genes involved in stress, inflammation, transcription and plasticity, and decreased mRNA levels of genes which control neurotransmitter function and ionic balance. In addition to a number of established ischemia-related genes, many genes not previously implicated in transient focal ischemia-induced brain damage [suppressor of cytokine signaling (SOCS)-3, cAMP responsive element modulator (CREM), cytosolic retinol binding protein (CRBP), silencer factor-B, survival motor neuron (SMN), interferon-gamma regulatory factor-1 (IRF-1), galanin, neurotrimin, proteasome subunit RC8, synaptosomal-associated protein (SNAP)-25 A and B, synapsin 1a, neurexin 1-beta, ras-related rab3, vesicular GABA transporter (VGAT), digoxin carrier protein, neuronal calcium sensor-1 and neurodap] were observed to be altered in the ischemic cortex. Real-time PCR confirmed the GeneChip results for several of these transcripts. SOCS-3 is a gene up-regulated after ischemia which modulates inflammation by controlling cytokine levels. Antisense knockdown of ischemia-induced SOCS-3 protein expression exacerbated transient MCAO-induced infarct volume assigning a neuroprotective role to SOCS-3, a gene not heretofore implicated in ischemic neuronal damage.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Reperfusion Injury  ISOIrf1 (Rattus norvegicus)632385; 632385mRNA:increased expression:cerebral cortexRGD 
Reperfusion Injury  IEP 632385mRNA:increased expression:cerebral cortexRGD 
Reperfusion Injury  ISOSocs3 (Rattus norvegicus)632385; 632385associated with Brain Ischemia more ...RGD 
Reperfusion Injury  IDA 632385associated with Brain Ischemia more ...RGD 
transient cerebral ischemia  ISOCrem (Rattus norvegicus)632385; 632385mRNA:increased expression:cerebral cortex (rat)RGD 
transient cerebral ischemia  IEP 632385mRNA:increased expression:cerebral cortex (rat)RGD 
transient cerebral ischemia  ISONrxn1 (Rattus norvegicus)632385; 632385associated with Hypertension and mRNA:decreased expression:cerebral cortexRGD 
transient cerebral ischemia  IEP 632385associated with Hypertension and mRNA:decreased expression:cerebral cortexRGD 

Objects Annotated

Genes (Rattus norvegicus)
Crem  (cAMP responsive element modulator)
Irf1  (interferon regulatory factor 1)
Nrxn1  (neurexin 1)
Socs3  (suppressor of cytokine signaling 3)

Genes (Mus musculus)
Crem  (cAMP responsive element modulator)
Irf1  (interferon regulatory factor 1)
Nrxn1  (neurexin I)
Socs3  (suppressor of cytokine signaling 3)

Genes (Homo sapiens)
CREM  (cAMP responsive element modulator)
IRF1  (interferon regulatory factor 1)
NRXN1  (neurexin 1)
SOCS3  (suppressor of cytokine signaling 3)


Additional Information