| pubmed-article:19531375 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19531375 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:19531375 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:19531375 | lifeskim:mentions | umls-concept:C0917798 | lld:lifeskim |
| pubmed-article:19531375 | lifeskim:mentions | umls-concept:C1865138 | lld:lifeskim |
| pubmed-article:19531375 | lifeskim:mentions | umls-concept:C0205234 | lld:lifeskim |
| pubmed-article:19531375 | lifeskim:mentions | umls-concept:C0205374 | lld:lifeskim |
| pubmed-article:19531375 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:19531375 | pubmed:dateCreated | 2009-8-17 | lld:pubmed |
| pubmed-article:19531375 | pubmed:abstractText | Cerebral ischemia/reperfusion injury is characterized by the development of inflammatory response, in which vascular macrophages and endogenous microglia are involved. Recent studies showed marked induction of hematopoietic prostaglandin D synthase (HPGDS) after ischemic/reperfusion injury and its localization in microglia, but the molecular mechanism(s) of HPGDS actions in cerebral ischemia is not clear. To clarify the role of HPGDS in cerebral ischemia, C57BL/6 mice and bone marrow chimera mice with cerebral ischemia/reperfusion injury were treated with (4-benzhydryloxy-(1) {3-(1H-tetrazol-5-yl)-propyl}piperidine (HQL-79), a specific inhibitor of HPGDS. The bone marrow chimera mice exhibit expression of enhanced green fluorescent protein (EGFP) in bone marrow/blood-derived monocytes/macrophages. Mice were subjected to ischemia/reperfusion and either treated with HQL-79 (n=44) or vehicle (n=44). Brain sections prepared at 72 h and 7 days after reperfusion were analyzed for neuronal nuclei (NeuN), HPGDS, ionized calcium-binding adapter molecule 1 (Iba1), inducible NO synthase (iNOS), nitrotyrosine, nuclear factor kappa B (NF-kB) and cyclooxygenase-2 (COX-2). The mortality rate (80%) and infarct size were larger in HQL-79- than vehicle-treated mice (58.7+/-8.5 versus 45.2+/-4.9 mm(3); mean+/-SEM, P<0.0001) at 7 days after reperfusion. HQL-79 reduced NeuN expression in the transition area and Iba1 expression (P<0.0001) in the ischemic peri- and penumbra area, but increased COX-2 (P<0.05) and NF-kB expression (P<0.05) in ischemic penumbra and increased formation of nitrotyrosine (P<0.0001) and iNOS (P<0.0001) in the ischemic core area at 72 h and 7 days after reperfusion. In EGFP chimera mice, HQL-79 increased the migration of Iba1/EGFP-positive bone marrow-derived monocytes/macrophages, and simultaneously upregulated iNOS expression in the ischemic core area (P<0.0001), but increased intrinsic microglia/macrophages in ischemic peri-area and penumbra (P<0.0001) at 72 h and 7 days after reperfusion, suggesting involvement of monocytes/macrophages in HQL-79-induced expansion of ischemic injury. Our results demonstrated that the neuroprotective effects of HPGDS in our model are mediated by suppression of activation and infiltration of inflammatory cells. | lld:pubmed |
| pubmed-article:19531375 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19531375 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19531375 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19531375 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19531375 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:19531375 | pubmed:issn | 1873-7544 | lld:pubmed |
| pubmed-article:19531375 | pubmed:author | pubmed-author:LinDD | lld:pubmed |
| pubmed-article:19531375 | pubmed:author | pubmed-author:HattoriNN | lld:pubmed |
| pubmed-article:19531375 | pubmed:author | pubmed-author:YamasakiYY | lld:pubmed |
| pubmed-article:19531375 | pubmed:author | pubmed-author:EguchiNN | lld:pubmed |
| pubmed-article:19531375 | pubmed:author | pubmed-author:UradeYY | lld:pubmed |
| pubmed-article:19531375 | pubmed:author | pubmed-author:UrabeTT | lld:pubmed |
| pubmed-article:19531375 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19531375 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:19531375 | pubmed:volume | 163 | lld:pubmed |
| pubmed-article:19531375 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19531375 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19531375 | pubmed:pagination | 296-307 | lld:pubmed |
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| pubmed-article:19531375 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19531375 | pubmed:articleTitle | Protective role of hematopoietic prostaglandin D synthase in transient focal cerebral ischemia in mice. | lld:pubmed |
| pubmed-article:19531375 | pubmed:affiliation | Research Institute for Disease of Old Age, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan. | lld:pubmed |
| pubmed-article:19531375 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19531375 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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