| pubmed-article:10754327 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10754327 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:10754327 | lifeskim:mentions | umls-concept:C0079460 | lld:lifeskim |
| pubmed-article:10754327 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:10754327 | lifeskim:mentions | umls-concept:C0031621 | lld:lifeskim |
| pubmed-article:10754327 | lifeskim:mentions | umls-concept:C0600388 | lld:lifeskim |
| pubmed-article:10754327 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:10754327 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:10754327 | lifeskim:mentions | umls-concept:C0205421 | lld:lifeskim |
| pubmed-article:10754327 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:10754327 | pubmed:dateCreated | 2000-5-9 | lld:pubmed |
| pubmed-article:10754327 | pubmed:abstractText | Activated neutrophils play an important role in the pathogenesis of sepsis, glomerulonephritis, acute renal failure, and other inflammatory processes. The resolution of neutrophil-induced inflammation relies, in large part, on removal of apoptotic neutrophils. Neutrophils are constitutively committed to apoptosis, but inflammatory mediators, such as GM-CSF, slow neutrophil apoptosis by incompletely understood mechanisms. We addressed the hypothesis that GM-CSF delays neutrophil apoptosis by activation of extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI 3-kinase) pathways. GM-CSF (20 ng/ml) significantly inhibited neutrophil apoptosis (GM-CSF, 32 vs 65% of cells p < 0. 0001). GM-CSF activated the PI 3-kinase/Akt pathway as determined by phosphorylation of Akt and BAD. GM-CSF-dependent Akt and BAD phosphorylation was blocked by the PI 3-kinase inhibitor LY294002. A role for the PI 3-kinase/Akt pathway in GM-CSF-stimulated delay of apoptosis was indicated by the ability of LY294002 to attenuate apoptosis delay. GM-CSF-dependent inhibition of apoptosis was significantly attenuated by PD98059, an ERK pathway inhibitor. LY294002 and PD98059 did not produce additive inhibition of apoptosis delay. To determine whether PI 3-kinase and ERK are used by other ligands that delay neutrophil apoptosis, we examined the role of these pathways in IL-8-induced apoptosis delay. LY294002 blocked IL-8-dependent Akt phosphorylation. PD98059 and LY294002 significantly attenuated IL-8 delay of apoptosis. These results indicate IL-8 and GM-CSF act, in part, to delay neutrophil apoptosis by stimulating PI 3-kinase and ERK-dependent pathways. | lld:pubmed |
| pubmed-article:10754327 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10754327 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10754327 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:10754327 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10754327 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10754327 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:10754327 | pubmed:author | pubmed-author:McLeishK RKR | lld:pubmed |
| pubmed-article:10754327 | pubmed:author | pubmed-author:KleinJ BJB | lld:pubmed |
| pubmed-article:10754327 | pubmed:author | pubmed-author:ScherzerJ AJA | lld:pubmed |
| pubmed-article:10754327 | pubmed:author | pubmed-author:KettritzRR | lld:pubmed |
| pubmed-article:10754327 | pubmed:author | pubmed-author:RangM LML | lld:pubmed |
| pubmed-article:10754327 | pubmed:author | pubmed-author:CoxonP YPY | lld:pubmed |
| pubmed-article:10754327 | pubmed:author | pubmed-author:MathiesenJ... | lld:pubmed |
| pubmed-article:10754327 | pubmed:author | pubmed-author:BuridiAA | lld:pubmed |
| pubmed-article:10754327 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10754327 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:10754327 | pubmed:volume | 164 | lld:pubmed |
| pubmed-article:10754327 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10754327 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10754327 | pubmed:pagination | 4286-91 | lld:pubmed |
| pubmed-article:10754327 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:10754327 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10754327 | pubmed:articleTitle | Granulocyte-macrophage colony-stimulating factor delays neutrophil constitutive apoptosis through phosphoinositide 3-kinase and extracellular signal-regulated kinase pathways. | lld:pubmed |
| pubmed-article:10754327 | pubmed:affiliation | Kidney Disease Program and Department of Biochemistry and Molecular Biology, University of Louisville and Veterans Affairs Medical Center, Louisville, KY 40292, USA. jon.klein@louisville.edu | lld:pubmed |
| pubmed-article:10754327 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10754327 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:10754327 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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