rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
1-2
|
pubmed:dateCreated |
2004-3-29
|
pubmed:abstractText |
Mice that lack tumor necrosis factor-alpha (TNF) receptors are more susceptible than wild-type animals to brain injury produced by kainic acid or transient focal ischemia suggesting that the rapid production of TNF that occurs after these insults serves a neuroprotective role. The mechanisms by which TNF reduces neuronal loss after brain injury may involve the up-regulation of proteins that maintain calcium homeostasis or reduce free radical generation. We report here that systemic administration of kainic acid rapidly elevates expression of mRNA encoding neuronal apoptosis inhibitor protein (NAIP) in the hippocampus and that this increase does not occur in mice that lack TNF receptors. Given that NAIP overexpression can reduce neuronal injury by blocking apoptosis, our findings suggest that induction of the naip gene may contribute to the neuroprotective properties of TNF.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Birc1a protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Kainic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Neuronal Apoptosis-Inhibitory...,
http://linkedlifedata.com/resource/pubmed/chemical/Neuroprotective Agents,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
0169-328X
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
7
|
pubmed:volume |
123
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
126-31
|
pubmed:dateRevised |
2005-11-17
|
pubmed:meshHeading |
pubmed-meshheading:15046874-Animals,
pubmed-meshheading:15046874-Apoptosis,
pubmed-meshheading:15046874-Brain Ischemia,
pubmed-meshheading:15046874-Disease Models, Animal,
pubmed-meshheading:15046874-Genetic Predisposition to Disease,
pubmed-meshheading:15046874-Hippocampus,
pubmed-meshheading:15046874-Kainic Acid,
pubmed-meshheading:15046874-Mice,
pubmed-meshheading:15046874-Mice, Knockout,
pubmed-meshheading:15046874-Nerve Degeneration,
pubmed-meshheading:15046874-Nerve Tissue Proteins,
pubmed-meshheading:15046874-Neuronal Apoptosis-Inhibitory Protein,
pubmed-meshheading:15046874-Neuroprotective Agents,
pubmed-meshheading:15046874-RNA, Messenger,
pubmed-meshheading:15046874-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:15046874-Tumor Necrosis Factor-alpha
|
pubmed:year |
2004
|
pubmed:articleTitle |
Kainic acid-induced naip expression in the hippocampus is blocked in mice lacking TNF receptors.
|
pubmed:affiliation |
Ottawa Hospital Research Institute, Faculty of Medicine, University of Ottawa, 451 Smyth Road, Ottawa, Ontario, Canada K1H 8M5.
|
pubmed:publicationType |
Journal Article
|