Source:http://linkedlifedata.com/resource/pubmed/id/16049425
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2006-2-24
|
| pubmed:abstractText |
Cerebral ischemia induces the expression of several growth factors and cytokines, which protect neurons against ischemic insults. Recent studies showed that granulocyte colony-stimulating factor (G-CSF) has a neuroprotective effect through the signaling pathway for the antiapoptotic cascade. The current study was designed to assess the neuroprotective mechanisms of G-CSF in ischemia/reperfusion injury using bone marrow chimera mice known to express enhanced green fluorescent protein (EGFP). Mice were subjected to ischemia/reperfusion and divided into two groups: those treated with G-CSF (G-CSF group) and vehicle (control group) (n = 35 in each group). Immunohistochemistry and immunoblotting for antiapoptotic protein, nitrotyrosine, and inducible nitrate oxide synthase (iNOS) were performed. G-CSF significantly reduced stroke volume (34%, P < 0.006). G-CSF upregulated Stat3, pStat3, and Bcl-2 (P < 0.05), and suppressed iNOS and nitrotyrosine expression. In EGFP chimera mice, G-CSF decreased the migration of Iba-1/EGFP-positive bone marrow-derived monocytes/macrophages and increased intrinsic microglia/macrophages at ischemic penumbra (P < 0.05), suggesting that bone marrow-derived monocytes/macrophages are not involved in G-CSF-induced reduction of ischemic injury size. Our study indicated that G-CSF exerts a neuroprotective effect through the direct activation of antiapoptotic pathway, and suggested that G-CSF is important for expansion of the therapeutic time window in patients with cerebral ischemia.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Granulocyte Colony-Stimulating...,
http://linkedlifedata.com/resource/pubmed/chemical/Neuroprotective Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Stat3 protein, mouse
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0271-678X
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
26
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
402-13
|
| pubmed:dateRevised |
2011-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:16049425-Animals,
pubmed-meshheading:16049425-Disease Models, Animal,
pubmed-meshheading:16049425-Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:16049425-Humans,
pubmed-meshheading:16049425-Ischemic Attack, Transient,
pubmed-meshheading:16049425-Macrophages,
pubmed-meshheading:16049425-Male,
pubmed-meshheading:16049425-Mice,
pubmed-meshheading:16049425-Mice, Inbred C57BL,
pubmed-meshheading:16049425-Mice, Transgenic,
pubmed-meshheading:16049425-Microglia,
pubmed-meshheading:16049425-Monocytes,
pubmed-meshheading:16049425-Neuroprotective Agents,
pubmed-meshheading:16049425-Nitric Oxide Synthase Type II,
pubmed-meshheading:16049425-Recombinant Proteins,
pubmed-meshheading:16049425-Reperfusion Injury,
pubmed-meshheading:16049425-STAT3 Transcription Factor,
pubmed-meshheading:16049425-Survival Rate,
pubmed-meshheading:16049425-Time Factors
|
| pubmed:year |
2006
|
| pubmed:articleTitle |
Neuroprotective effect of recombinant human granulocyte colony-stimulating factor in transient focal ischemia of mice.
|
| pubmed:affiliation |
Department of Neurology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|