کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9886588 | 1537838 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Stress-induced platelet-activating factor synthesis in human neutrophils
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کلمات کلیدی
PBSERK-1/2GPCHBSSPLA2LC-MS/MS - LC-MS / MSMAPK - MAPKMS/MS - MS / MSp38 MAPK - P38 MAPKphospholipase A2 - آنزیم فسفولیپاز A2 Stress - استرس یا فشار روانیacetyltransferase - استیل ترانسفرازsn-glycero-3-phosphocholine - اسپیگلیسرو-3 فسفو سولینTandem mass spectrometry - طیف سنجی جرمی پشت سر هم یا متوالیPlatelet-activating factor - فاکتور فعال کننده پلاکتneutrophil - نوتروفیلPAF - نیروی هوایی پاکستانmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenliquid chromatography coupled to tandem mass spectrometry - کروماتوگرافی مایع همراه با طیف سنجی جرمی دو طرفه
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine; PAF) is a potent inflammatory mediator produced by cells in response to physical or chemical stress. The mechanisms linking cell injury to PAF synthesis are unknown. We used liquid chromatography-tandem mass spectrometry to investigate stress-induced PAF synthesis in human neutrophils. PAF synthesis induced by extracellular pH 5.4 correlated with the activation of a stress-activated kinase, p38 mitogen-activated protein kinase (MAPK), and was blocked by the p38 MAPK inhibitor SB 203580. A key enzyme of PAF synthesis, acetyl-CoA:lysoPAF acetyltransferase, which we have previously shown is a target of p38 MAPK, was also activated in an SB 203580-sensitive fashion. Another MAPK pathway, extracellular signal-regulated kinase-1/2 (ERK-1/2), was also activated. Surprisingly, the pharmacological blockade of the ERK-1/2 pathway with PD 98059 did not block, but rather enhanced, PAF accumulation. Two unexpected actions of PD 98059 may underlie this phenomenon: an augmentation of stress-induced p38 MAPK phosphorylation and an inhibition of PAF catabolism. The latter effect did not appear to be due to a direct inhibition of PAF acetylhydrolase. Finally, similar results were obtained using another form of cellular stress, hypertonic sodium chloride. These data are consistent with a model in which stress-induced PAF accumulation is regulated positively by p38 MAPK and negatively by ERK-1/2. Such a model contrasts with the PAF accumulation induced by other forms of stimulation, which we and others have found is up-regulated by both p38 MAPK and ERK-1/2.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1733, Issues 2â3, 15 April 2005, Pages 120-129
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1733, Issues 2â3, 15 April 2005, Pages 120-129
نویسندگان
John S. Owen, Paul R.S. Baker, Joseph T. O'Flaherty, Michael J. Thomas, Michael P. Samuel, Rhonda E. Wooten, Robert L. Wykle,