Source:http://linkedlifedata.com/resource/pubmed/id/11376856
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2001-5-29
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| pubmed:abstractText |
Interleukin-1beta (IL-1beta) upregulates expression of the chemokine monocyte chemoattractant protein-1 (MCP-1) in many experimental models. In neonatal rodent brain, hypoxia-ischemia rapidly stimulates expression of this chemokine, although the role of IL-1beta in regulating this response is unknown. Interleukin-1 converting enzyme (ICE) is a cysteine protease that cleaves inactive pro-IL-1beta to generate mature IL-1beta. Neonatal mice with a homozygous deletion of ICE (ICE -/-) are resistant to moderate, but not to severe cerebral hypoxic-ischemic insults, relative to their wild-type controls. We hypothesized that their resistance to moderate hypoxic-ischemic insults is mediated by suppression of the acute inflammatory response to brain injury in the absence of IL-1beta, and that hypoxia-ischemia induced MCP-1 expression would be attenuated in ICE -/- animals. To test this hypothesis, paired litters of 9-10-day-old ICE -/- and wild-type mice underwent right carotid ligation, followed by 40, 70 or 120 min exposure to 10% O2 and ischemia-induced changes in MCP-1 mRNA and protein were compared, using a semi-quantitative reverse-transcription polymerase chain reaction assay and an ELISA, respectively. With a lesioning protocol that elicits minimal injury in wild-types (ligation+40 min 10% O2), there was an attenuation of hypoxia-ischemia-induced MCP-1 production at 8 h post-hypoxia; in contrast, in animals that underwent longer periods of hypoxia-ischemia the magnitude of injury-induced induced MCP-1 production did not differ between wild-type and ICE -/- animals. These results demonstrate both that the acute inflammatory response to hypoxia-ischemia is attenuated in ICE -/- animals, and also that hypoxic-ischemic brain injury stimulates MCP-1 expression even in the absence of IL-1beta activity.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
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| pubmed:issn |
0169-328X
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
20
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| pubmed:volume |
90
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
57-67
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:11376856-Animals,
pubmed-meshheading:11376856-Animals, Newborn,
pubmed-meshheading:11376856-Apoptosis,
pubmed-meshheading:11376856-Asphyxia Neonatorum,
pubmed-meshheading:11376856-Brain,
pubmed-meshheading:11376856-Carotid Arteries,
pubmed-meshheading:11376856-Caspase 1,
pubmed-meshheading:11376856-Chemokine CCL2,
pubmed-meshheading:11376856-Disease Models, Animal,
pubmed-meshheading:11376856-Female,
pubmed-meshheading:11376856-Gene Expression Regulation,
pubmed-meshheading:11376856-Humans,
pubmed-meshheading:11376856-Hypoxia-Ischemia, Brain,
pubmed-meshheading:11376856-Infant, Newborn,
pubmed-meshheading:11376856-Inflammation,
pubmed-meshheading:11376856-Interleukin-1,
pubmed-meshheading:11376856-Ligation,
pubmed-meshheading:11376856-Male,
pubmed-meshheading:11376856-Mice,
pubmed-meshheading:11376856-Mice, Knockout,
pubmed-meshheading:11376856-Nerve Tissue Proteins
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| pubmed:year |
2001
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| pubmed:articleTitle |
Attenuation of hypoxia-ischemia-induced monocyte chemoattractant protein-1 expression in brain of neonatal mice deficient in interleukin-1 converting enzyme.
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| pubmed:affiliation |
Department of Pediatrics, University of Michigan, Rm. 8301 MSRB3, Box 0646, 1150 W. Medical Center Dr., Ann Arbor, MI 48109-0646, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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