A new method of purification and sensitive bioassay of platelet- activating factor (PAF) in human whole blood

Shinozaki, Koji; Kawasaki, Tomio; Kambayashi, Jun-ichi; Sakon, Masato; Shiba, Eiichi; Uemura, Yoshio; Ou, Ming-Che; Iwamoto, Noriko; Mori, Takesada

doi:10.1016/0024-3205(94)00701-2

Cited by 9 publications

(4 citation statements)

References 20 publications

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“…76 Some studies have found increased serum PAF levels in septic patients, 79,80 but others have found no significant increase compared with levels in healthy control subjects. 81,82 Plasma PAF-AH activity has also been found to be decreased in some patients with sepsis, raising the possibility of a pathogenic imbalance between increased PAF generation and decreased degradation. 46 A short-term analysis of patients with acute lung injury and acute respiratory distress syndrome predominantly caused by sepsis found that nonsurvivors had significantly lower plasma PAF-AH activity than survivors.…”

Section: Allergic Rhinitis and Asthmamentioning

confidence: 97%

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Gill

Jindal

Jagdis

et al. 2015

Journal of Allergy and Clinical Immunology

106

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Anaphylaxis is an acute, severe, life-threatening multisystem allergic reaction resulting from the sudden systemic release of biochemical mediators and chemotactic substances. Release of both preformed granule-associated mediators and newly generated lipid-derived mediators contributes to the amplification and prolongation of anaphylaxis. Platelet-activating factor (PAF) is a potent phospholipid-derived mediator the central role of which has been well established in experimental models of both immune-mediated and non-immune mediated anaphylaxis. It is produced and secreted by several types of cells, including mast cells, monocytes, tissue macrophages, platelets, eosinophils, endothelial cells, and neutrophils. PAF is implicated in platelet aggregation and activation through release of vasoactive amines in the inflammatory response, resulting in increased vascular permeability, circulatory collapse, decreased cardiac output, and various other biological effects. PAF is rapidly hydrolyzed and degraded to an inactive metabolite, lysoPAF, by the enzyme PAF acetylhydrolase, the activity of which has shown to correlate inversely with PAF levels and predispose to severe anaphylaxis. In addition to its role in anaphylaxis, PAF has also been implicated as a mediator in both allergic and nonallergic inflammatory diseases, including allergic rhinitis, sepsis, atherosclerotic disease, and malignancy, in which PAF signaling has an established role. The therapeutic role of PAF antagonism has been investigated for several diseases, with variable results thus far. Further investigation of its role in pathology and therapeutic modulation is highly anticipated because of the pressing need for more selective and targeted therapy for the management of severe anaphylaxis.

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Section: Allergic Rhinitis and Asthmamentioning

confidence: 97%

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Gill

Jindal

Jagdis

et al. 2015

Journal of Allergy and Clinical Immunology

106

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“…The PAF assay was performed according to previous studies (15,16). For analysis of PAF concentration in NSCLC cell lines, cells were washed thrice with Hank balanced salt solution.…”

Section: Paf Assaymentioning

confidence: 99%

Feed-Forward Reciprocal Activation of PAFR and STAT3 Regulates Epithelial–Mesenchymal Transition in Non–Small Cell Lung Cancer

et al. 2015

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Platelet-activating factor receptor (PAFR), a G-protein-coupled receptor, has been implicated in tumorigenesis, but its contributions to metastatic progression have not been investigated. Here, we show that PAFR is overexpressed in non-small cell lung cancer (NSCLC) as well as in breast, colorectal, and gastric carcinomas. Expression of PAFR correlates closely with clinical stages, survival time, and distant metastasis. In human NSCLC cells, activation of the PAF/PAFR signaling axis accentuated malignant character, including by stimulating epithelial-mesenchymal transition (EMT). In contrast, silencing PAFR in aggressive NSCLC cells inhibited these effects. Mechanistic investigations showed that PAFR stimulated EMT by activating STAT3 via upregulation of G-protein-dependent SRC or JAK2 kinase activity. Notably, STAT3 transcriptionally elevated PAFR expression. Thus, activation of PAFR in NSCLC cells initiated a forward feedback loop responsible for mediating the aggressive malignant character of NSCLC cells in vitro and in vivo. Reinforcing this reciprocal activation loop, PAF/PAFR signaling also upregulated IL6 expression and thereby STAT3 activation. Overall, our results elucidated an important role for PAFR dysregulation in the pathogenicity of NSCLC and unraveled a forward feedback loop between PAFR and STAT3 that acts to drive the malignant progression of NSCLC. Cancer Res; 75(19); 4198-210. Ó2015 AACR.

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“…For the analysis of PAF level in ESCC tissues, 12 paired clinical ESCC tissues and their matched adjacent normal tissues were homogenized in 9.5 ml of methanol, chloroform and deionized water (2:1:0.8, v/v), respectively. 47,48 For the analysis of PAF concentration in ESCC cell lines, cells were washed three times with HBSS. The released and the cell-associated PAFs were extracted from supernatants and cells by mixing supernatants and cells in 9.5 ml of methanol, chloroform and deionized water (2:1:0.8, v/v).…”

Section: Real-time Rt-pcrmentioning

confidence: 99%

Platelet-activating factor receptor-mediated PI3K/AKT activation contributes to the malignant development of esophageal squamous cell carcinoma

Lan

Zhang

et al. 2015

Oncogene

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Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies worldwide and occurs at a relatively high frequency in China, yet the mechanisms underlying its devastating outcome remain unclear. Here we report that platelet-activating factor receptor (PAFR), a type of G-protein-coupled receptor, was upregulated in ESCC tumors and cell lines, compared with controls; PAFR levels were positively correlated with ESCC clinical stages and survival time. Overexpression of PAFR promoted the malignant development of ESCC in vitro and in vivo, whereas depletion of PAFR suppressed these effects. Interestingly, PAFR was observed to activate PI3K/AKT (phosphatidylinositol 3-kinase/AKT) through the upregulation of FAK kinase activity. AKT-triggered nuclear factor-κB transcriptionally activated PAFR expression. This mutual positive regulation between PAFR and AKT was required for the aggressiveness of ESCC cells both in vitro and in vivo. Furthermore, treating mice bearing ESCC tumors with cholesterol-conjugated PAFR small interfering RNA effectively inhibited tumor progression and the expression of AKT-mediated oncogenic proteins. Taken together, we made the first demonstration that dysregulation of PAFR and the positive regulatory loop between PAFR and pAKT contribute to malignant progression of ESCC.

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A new method of purification and sensitive bioassay of platelet- activating factor (PAF) in human whole blood

Cited by 9 publications

References 20 publications

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

Feed-Forward Reciprocal Activation of PAFR and STAT3 Regulates Epithelial–Mesenchymal Transition in Non–Small Cell Lung Cancer

Platelet-activating factor receptor-mediated PI3K/AKT activation contributes to the malignant development of esophageal squamous cell carcinoma

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