cDNA Cloning of Human Cytosolic Platelet-Activating Factor Acetylhydrolase γ-Subunit and Its mRNA Expression in Human Tissues

1995 ◽  
Vol 214 (1) ◽  
pp. 180-187 ◽  
Author(s):  
H. Adachi ◽  
M. Tsujimoto ◽  
M. Hattori ◽  
H. Arai ◽  
K. Inoue
Keyword(s):  
Mrna Expression ◽  
Cdna Cloning ◽  
Platelet Activating Factor ◽  
Human Tissues ◽  
Platelet Activating Factor Acetylhydrolase ◽  
Γ Subunit

In vivo regulation of plasma platelet-activating factor acetylhydrolase during the acute phase response

1999 ◽  
Vol 277 (1) ◽  
pp. R94-R103 ◽  
Author(s):  
Riaz A. Memon ◽  
John Fuller ◽  
Arthur H. Moser ◽  
Kenneth R. Feingold ◽  
Carl Grunfeld
Keyword(s):  
Mrna Expression ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Platelet Activating Factor ◽  
Phase Response ◽  
Mrna Levels ◽  
Potent Inducer ◽  
Platelet Activating Factor Acetylhydrolase ◽  
Infection And Inflammation ◽  
Lps Treatment

Plasma platelet-activating factor acetylhydrolase (PAF-AH) hydrolyzes PAF and oxidized phospholipids and is associated with lipoproteins in the circulation. Endotoxin [lipopolysaccharide (LPS)], a potent inducer of the acute phase response (APR), produces marked changes in several proteins that play important roles in lipoprotein metabolism. We now demonstrate that LPS produces a 2.5- to 3-fold increase in plasma PAF-AH activity in Syrian hamsters. The plasma PAF-AH activity is found in the high-density lipoprotein (HDL) fraction and is increased threefold with LPS treatment despite a decrease in plasma HDL levels, indicating that plasma PAF-AH activity is increased per HDL particle. LPS markedly increased PAF-AH mRNA levels in liver, spleen, lung, and small intestine. The maximal increase in plasma PAF-AH activity and mRNA expression in liver and spleen is seen 24 h after LPS treatment. Both tumor necrosis factor and interleukin-1 modestly increased plasma PAF-AH activity and mRNA levels in liver and spleen, suggesting that they may partly mediate the effect of LPS on PAF-AH. Surgical removal of spleen had no effect on basal or LPS-induced plasma PAF-AH activity, suggesting that spleen per se may not contribute to plasma PAF-AH activity. Finally, LPS, turpentine and zymosan increased plasma PAF-AH activity in mice and/or rats, indicating that multiple APR inducers upregulate plasma PAF-AH and this effect is consistent across different rodent species. Taken together, our results indicate that plasma PAF-AH activity and mRNA expression is markedly upregulated during the host response to infection and inflammation. An increase in plasma PAF-AH may enhance the degradation of PAF as well as alter the structure and function of HDL during infection and inflammation.

Platelet-activating factor acetylhydrolase activity in human tissues and blood cells

Lipids ◽  
1991 ◽  
Vol 26 (12) ◽  
pp. 979-985 ◽  
Author(s):  
Diana M. Stafforini ◽  
Stephen M. Prescott ◽  
Guy A. Zimmerman ◽  
Thomas M. McIntyre
Keyword(s):  
Blood Cells ◽  
Platelet Activating Factor ◽  
Human Tissues ◽  
Platelet Activating Factor Acetylhydrolase

A Mutation in Plasma Platelet-activating Factor Acetylhydrolase (Val279Phe) Is a Genetic Risk Factor for Cerebral Hemorrhage but not for Hypertension

1998 ◽  
Vol 80 (09) ◽  
pp. 372-375 ◽  
Author(s):  
Hidemi Yoshida ◽  
Tadaatsu Imaizumi ◽  
Koji Fujimoto ◽  
Hiroyuki Itaya ◽  
Makoto Hiramoto ◽  
...  
Keyword(s):  
Risk Factor ◽  
Genetic Risk ◽  
Platelet Activating Factor ◽  
Vascular Diseases ◽  
Genetic Risk Factor ◽  
Brain Hemorrhage ◽  
Platelet Activating Factor Acetylhydrolase ◽  
Paf Acetylhydrolase ◽  
Polymerase Chain ◽  
The Difference

SummaryPlatelet-activating factor (PAF) acetylhydrolase is an enzyme that inactivates PAF. Deficiency of this enzyme is caused by a missense mutation in the gene. We previously found a higher prevalence of this mutation in patients with ischemic stroke. This fact suggests that the mutation might enhance the risk for stroke through its association with hypertension. We have addressed this hypothesis by analyzing the prevalence of the mutation in hypertension. We studied 138 patients with essential hypertension, 99 patients with brain hemorrhage, and 270 healthy controls. Genomic DNA was analyzed for the mutant allele by the polymerase-chain reaction. The prevalence of the mutation was 29.3% (27.4% heterozygotes and 1.9% homozygotes) in controls and 36.2% in hypertensives and the difference was not significant. The prevalence in patients with brain hemorrhage was significantly higher than the control: 32.6% heterozygotes and 6.1% homozygotes (p <0.05). PAF acetylhydrolase deficiency may be a genetic risk factor for vascular diseases.

scholarly journals Consumption of Enriched Yogurt with PAF Inhibitors from Olive Pomace Affects the Major Enzymes of PAF Metabolism: A Randomized, Double Blind, Three Arm Trial

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 801
Author(s):  
Maria Detopoulou ◽  
Agathi Ntzouvani ◽  
Filio Petsini ◽  
Labrini Gavriil ◽  
Εlizabeth Fragopoulou ◽  
...  
Keyword(s):  
Platelet Activating Factor ◽  
Lipid Mediator ◽  
Olive Pomace ◽  
Double Blind ◽  
Promising Alternative ◽  
Catabolic Enzymes ◽  
Platelet Activating Factor Acetylhydrolase ◽  
The Impact ◽  
By Products ◽  
Apparently Healthy

Platelet-activating factor (PAF), a proinflammatory lipid mediator, plays a crucial role in the formation of the atherosclerotic plaque. Therefore, the inhibition of endothelium inflammation by nutraceuticals, such as PAF inhibitors, is a promising alternative for preventing cardiovascular diseases. The aim of the present study was to evaluate the impact of a new functional yogurt enriched with PAF inhibitors of natural origin from olive oil by-products on PAF metabolism. Ninety-two apparently healthy, but mainly overweight volunteers (35–65 years) were randomly allocated into three groups by block-randomization. The activities of PAF’s biosynthetic and catabolic enzymes were measured, specifically two isoforms of acetyl-CoA:lyso-PAF acetyltransferase (LPCATs), cytidine 5′-diphospho-choline:1-alkyl-2-acetyl-sn-glycerol cholinephosphotransferase (PAF-CPT) and two isoforms of platelet activating factor acetylhydrolase in leucocytes (PAF-AH) and plasma (lipoprotein associated phospholipase-A2, LpPLA2). The intake of the enriched yogurt resulted in reduced PAF-CPT and LpPLA2 activities. No difference was observed in the activities of the two isoforms of lyso PAF-AT. In conclusion, intake of yogurt enriched in PAF inhibitors could favorably modulate PAF biosynthetic and catabolic pathways.

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