Oxidatively fragmented phosphatidylcholines activate human neutrophils through the receptor for platelet-activating factor

Smiley, Patricia L.; Stremler, Kay E.; Prescott, Stephen M.; Zimmerman, Guy A.; McIntyre, Thomas M.

doi:10.1016/s0021-9258(18)99133-7

Cited by 199 publications

(27 citation statements)

References 38 publications

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“…The involvement of free radicals in the formation of fragmented phospholipids has been well documented in vitro (16)(17)(18)27), but there is little direct evidence that this is also true in vivo. The free radical hypothesis was supported by the observation that cigarette smoke acutely increased the concentration of fragmented PC (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The pathology of oxygen toxicity is poorly understood, but inflammatory mediators such as PAF are potentially involved. Because fragmented phospholipids may have activities that resemble PAF (16)(17)(18)(19)(20), it can be hypothesized that they play a role in hyperoxic lung injury. Consistent with Fig.…”

Section: Discussionmentioning

confidence: 99%

“…One example of oxidative modification is acyl chain fragmentation. Fragmented phospholipids can be produced in vitro by oxidation of unsaturated phosphatidylcholine (PC) and were shown to activate neutrophils via the receptor for platelet-activating factor (PAF) (16). Moreover, peroxidation in vitro of isolated lipoproteins (17) and endothelial cell cultures (18) produced fragmented phospholipids that carried biological activities similar to PAF.…”

mentioning

confidence: 99%

“…Moreover, peroxidation in vitro of isolated lipoproteins (17) and endothelial cell cultures (18) produced fragmented phospholipids that carried biological activities similar to PAF. The chemical structure of this activity is not known; however, several synthetic PCs with short acyl chains had stimulatory effects on neutrophils (16), platelets (19,20), and monocytes (20).…”

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confidence: 99%

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Increase in fragmented phosphatidylcholine in blood plasma by oxidative stress

Frey

Haupt

Alms

et al. 2000

Journal of Lipid Research

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Oxidatively modified phospholipids with fragmented acyl chains have attracted much interest because of their proinflammatory activity and their potential involvement in atherosclerosis. They can be formed in vitro by free radical treatment of unsaturated phospholipids but it is not known under which conditions they accumulate in vivo. We assayed one species of fragmented phosphatidylcholine (PC) in human blood plasma by high performance liquid chromatography after precolumn derivatization with chloromethylanthracene. Structural analysis suggested that fragmented PC was a diacyl species with a palmitoyl group and a short oxidized residue, which most likely had four carbons. The concentration of fragmented PC was higher in elderly individuals with coronary heart disease than in young healthy controls. Smoking one cigarette acutely increased the concentration of fragmented PC in healthy adults. Fragmented PC also increased in the reperfusion period after treatment with cardiopulmonary bypass. The increase coincided with a surge of circulating neutrophils. In rats, the plasma concentration of fragmented PC was elevated by vitamin E deficiency and exposure to high oxygen.The data demonstrate that fragmented PC increases in blood plasma in response to various forms of oxidative stress. -Frey, B.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Increase in fragmented phosphatidylcholine in blood plasma by oxidative stress

Frey

Haupt

Alms

et al. 2000

Journal of Lipid Research

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“…Due to their structural similarity to the platelet activating factor (PAF) (reviewed in: ref. 17) these oxidized phospholipids can promote platelet aggregation (18), neutrophil activation (19), and leukocyte adhesion (20).…”

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confidence: 99%

Femtomole analysis of 9-oxononanoyl cholesterol by high performance liquid chromatography

Karten

Boechzelt

Abuja

et al. 1998

Journal of Lipid Research

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9-Oxononanoyl cholesterol, a cholesterol core-aldehyde formed during lipoprotein oxidation, was recently identified in advanced human atherosclerotic lesions. Here we present a rapid and sensitive HPLC method for 9-oxononanoyl cholesterol analysis. 9-Oxononanoyl cholesterol was converted to the corresponding fluorescent decahydroacridine derivative by reaction with 1,3-cyclohexanedione. The derivatives formed were purified by solid-phase extraction on C-18 columns, separated by reversed phase HPLC with isocratic elution, and detected by their fluorescence. Decahydroacridine derivatives of 9-oxononanoyl cholesterol were stable for at least 160 h. The limit of quantitation of the method presented is at the low ( Ϸ 50) femtomole level, with an absolute limit of detection (signal: noise ‫؍‬ 6) of 15 fmol. Intra-assay variation was Յ 5%, while interassay variations were between 5 and 15%, depending on the concentration of the analyte. Standard curves were linear over nearly three orders of magnitude (50 fmol-12.5 pmol). 9-Oxononanoyl cholesterol proved to be the major cholesterol core-aldehyde formed during t-BuOOH/FeSO 4 oxidation of cholesteryl linoleate and Cu 2 ϩ -induced LDL oxidation, findings confirmed by atmospheric pressure chemical ionization-mass spectrometry. Analysis of lipid extracts obtained from advanced human atherosclerotic lesions revealed the presence of 9-oxononanoyl cholesterol in all tissue samples analyzed (28 ؎ 14 mol/mol cholesterol, n ‫؍‬ 9) despite the presence of ␣ -tocopherol (4 ؎ 1.2 mmol/mol cholesterol, n ‫؍‬ 9).

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Recombinant plasma-type platelet-activating factor acetylhydrolase attenuates NMDA-induced hippocampal neuronal apoptosis

1998

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The bioactive lipid platelet-activating factor (PAF) accumulates in brain during injury, seizures and ischemia and may, in addition, be significant in AIDS dementia and in other neurodegenerative diseases. We have used plasma-type recombinant PAF acetylhydrolase (rPAF-AH) to test the hypothesis that PAF accumulation is involved in early events leading to neuronal apoptosis during excitotoxic neuronal injury. Neuronal cultures were labeled with FITC-12-dUTP (TUNEL technique) and propidium iodide, digitized using fluorescence microscopy and a chilled 3CCD color camera, and analyzed with 2D graphics analysis software. N-methyl-D-aspartate (NMDA) (50 microM, 2 hr) induced a 2.5-fold increase in apoptosis of hippocampal neurons compared with controls when analyzed 24 hr after NMDA treatment. Hippocampal neurons receiving rPAF-AH (20 microg/ml) before, during, and after NMDA treatment demonstrated a concentration-dependent neuroprotective effect which resulted in 47% and 30% neuroprotection against 50 and 100 microM NMDA, respectively. The noncompetitive NMDA receptor antagonist MK-801(300 nM) completely inhibited apoptosis caused by NMDA. The neuroprotective effect of rPAF-AH against NMDA-induced apoptosis was confirmed using as additional criteria, histone release, electron microscopy, and DNA laddering. Neuroprotection elicited by rPAF-AH demonstrates that PAF is an injury mediator in NMDA-induced neuronal apoptosis and that the recombinant protein is potentially useful as a therapeutic approach.

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Oxidatively fragmented phosphatidylcholines activate human neutrophils through the receptor for platelet-activating factor

Cited by 199 publications

References 38 publications

Increase in fragmented phosphatidylcholine in blood plasma by oxidative stress

Increase in fragmented phosphatidylcholine in blood plasma by oxidative stress

Femtomole analysis of 9-oxononanoyl cholesterol by high performance liquid chromatography

Recombinant plasma-type platelet-activating factor acetylhydrolase attenuates NMDA-induced hippocampal neuronal apoptosis

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