RGD Reference Report - Differential cellular expression of tumor necrosis factor-alpha and Type I tumor necrosis factor receptor after transient global forebrain ischemia. - Rat Genome Database

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Differential cellular expression of tumor necrosis factor-alpha and Type I tumor necrosis factor receptor after transient global forebrain ischemia.

Authors: Sairanen, T R  Lindsberg, P J  Brenner, M  Carpén, O  Sirén, A 
Citation: Sairanen TR, etal., J Neurol Sci. 2001 May 1;186(1-2):87-99.
RGD ID: 13825263
Pubmed: PMID:11412877   (View Abstract at PubMed)

We examined the expression of tumor necrosis factor-alpha (TNF-alpha) and the Type I tumor necrosis factor receptor, (TNFR1), in relation to c-fos, a known regulator gene of immediate cellular responses, after an extended period of global ischemia. The number of TNF-alpha mRNA expressing cells peaked in most brain areas after 8 h of reperfusion. Significant increases in TNFR1 mRNA expression were evident in the cortex at 2 and 8 h of reperfusion and after 8 h of reperfusion in the CA3/CA4 region of the hippocampus. Transient neuronal c-fos mRNA expression preceded these responses. TNF-alpha immunoreactivity was seen in neurons>oligodendrocytes=perivascular cells=ependymal cells=vessel wall structures. After ischemia/reperfusion, increased TNF-alpha immunoreactivity was evident only in oligodendrocytes. TNFR1 immunoreactivity in sham brains manifested in bundles of cellular fibers of variable length and thickness. In post-ischemic brains, immunoreactivity in these cellular processes representing mainly astroglial extensions was suppressed at 2 h but recovered partially by 8 and 24 h of reperfusion. In contradiction, transient ischemia-induced TNFR1 immunoreactivity was observed in somas of large cortical neurons, in activated microglia/macrophages, perivascular and endothelial cells.Taken together, the increase in neuronal TNF-alpha mRNA appeared not to be followed by substantial translation to protein in the cerebral tissue after an extended period of global ischemia. However, there was increased neuronal TNFR1 immunostaining in conjunction with increased immunostaining for TNF-alpha in oligoglial elements, which suggests signaling to neurons by enhanced oligoglial TNF-alpha.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
TNFHumantransient cerebral ischemia  ISOTnf (Rattus norvegicus)mRNA:increased expression:striatum and hippocampus:RGD 
TNFRSF1AHumantransient cerebral ischemia  ISOTnfrsf1a (Rattus norvegicus)mRNA:increased expression:striatum and hippocampus:RGD 
TnfRattransient cerebral ischemia  IEP mRNA:increased expression:striatum and hippocampus:RGD 
TnfMousetransient cerebral ischemia  ISOTnf (Rattus norvegicus)mRNA:increased expression:striatum and hippocampus:RGD 
Tnfrsf1aRattransient cerebral ischemia  IEP mRNA:increased expression:striatum and hippocampus:RGD 
Tnfrsf1aMousetransient cerebral ischemia  ISOTnfrsf1a (Rattus norvegicus)mRNA:increased expression:striatum and hippocampus:RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Cellular Component

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
TnfRatneuronal cell body  IDA mRNA:increased expression:striatum and hippocampus:RGD 

Objects Annotated

Genes (Rattus norvegicus)
Tnf  (tumor necrosis factor)
Tnfrsf1a  (TNF receptor superfamily member 1A)

Genes (Mus musculus)
Tnf  (tumor necrosis factor)
Tnfrsf1a  (tumor necrosis factor receptor superfamily, member 1a)

Genes (Homo sapiens)
TNF  (tumor necrosis factor)
TNFRSF1A  (TNF receptor superfamily member 1A)


Additional Information