| http://purl.uniprot.org/citations/12122053 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12122053 | http://www.w3.org/2000/01/rdf-schema#comment | "Inflammation is a critical factor for development of hypoxic-ischemic (HI) brain injury. Interleukin-18 (IL-18) is a proinflammatory cytokine expressed in microglia and processed by caspase-1. Our aim was to characterize the expression of IL-18 and its receptor in relation to caspase-1 and IL-1beta after HI and to evaluate to what extent IL-18 contributes to HI brain injury. Seven-day-old rats were subjected to HI, and brain tissue was sampled at different time points (3 hr to 14 d) after insult. The mRNA for IL-18 and caspase-1 were analyzed with reverse transcriptase PCR, protein was analyzed by Western blot (IL-18, caspase-1) or ELISA (IL-1beta), and the regional distribution was assessed by immunohistochemistry. HI was also induced in C57BL/6 mice, and brain injury in IL-18-deficient animals was compared with that in wild-type animals. The expression of mRNA/protein for caspase-1 and IL-18 in brain homogenates increased progressively at 12 hr to 14 d after HI, whereas IL-1beta peaked at 8 hr. A widespread expression of caspase-1 and IL-18 protein in microglia was found in the HI hemisphere. The IL-18 receptor was expressed on neurons of the cerebral cortex and thalamus. IL-1beta was primarily found in microglia in the habenular nucleus of the thalamus. The infarct volume was reduced by 21% (p = 0.01), and the neuropathology score was significantly decreased in the cerebral cortex (-35%), hippocampus (-22%), striatum (-18%), and thalamus (-17%) in mice with IL-18 deficiency compared with wild-type mice. In conclusion, we found that IL-18 expression in microglia was markedly increased after HI and that IL-18 appears to be important for the development of HI brain injury."xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.org/dc/terms/identifier | "doi:10.1523/jneurosci.22-14-05910.2002"xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/author | "Blomgren K."xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/author | "Hagberg H."xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/author | "Hedtjarn M."xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/author | "Eriksson K."xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/author | "Leverin A.L."xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/author | "Mallard C."xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/name | "J Neurosci"xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/pages | "5910-5919"xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/title | "Interleukin-18 involvement in hypoxic-ischemic brain injury."xsd:string |
| http://purl.uniprot.org/citations/12122053 | http://purl.uniprot.org/core/volume | "22"xsd:string |
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