Transcellular biosynthesis of eicosanoid lipid mediators

Capra, Valérie; Rovati, G. Enrico; Mangano, Paolo; Buccellati, Carola; Murphy, Robert C.; Sala, Angelo

doi:10.1016/j.bbalip.2014.09.002

Cited by 77 publications

(68 citation statements)

References 80 publications

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“…Once released, AA can be metabolized by 3 main pathways: the COX pathway that produces prostanoids, the lipoxygenase (LOX) pathway that produces leukotrienes and lipoxins, and the P‐450 epoxygenase pathway that produces epoxides 16. The erythrocyte membrane is a rich source of AA, but lacks both the COX and LOX enzymes, and therefore cannot produce the majority of eicosanoids 18. However, the AA‐rich erythrocytes can contribute to eicosanoid synthesis by transcellular biosynthesis (ie, the cooperation of different cell types to produce eicosanoids).…”

Section: Discussionmentioning

confidence: 99%

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Effects of Leukoreduction and Storage on Erythrocyte Phosphatidylserine Expression and Eicosanoid Concentrations in Units of Canine Packed Red Blood Cells

Muro

Lee

Ross

et al. 2017

Veterinary Internal Medicne

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BackgroundStorage of canine packed red blood cells (pRBCs) can increase erythrocyte phosphatidylserine (PS) expression and eicosanoid concentrations.Hypothesis/ObjectivesTo determine the effects of leukoreduction on erythrocyte PS expression and eicosanoid concentrations in stored units of canine pRBCs. Our hypothesis was that leukoreduction would decrease PS expression and eicosanoid concentrations.AnimalsEight healthy dogs.MethodsIn a cross‐over study, units of whole blood were leukoreduced (LR) or non‐LR and stored (10 and 21 days) as pRBCs. Samples were collected at donation, and before and after a simulated transfusion. PS expression was measured by flow cytometry, and concentrations of arachidonic acid (AA), prostaglandin F2α (PGF 2α), prostaglandin E2 (PGE 2), prostaglandin D2 (PGD 2), thromboxane B2 (TXB 2), 6‐keto‐prostaglandin F1α (6‐keto‐PGF 1α), and leukotriene B4 (LTB 4) were quantified by liquid chromatography–mass spectrometry.ResultsThere was no change in PS expression during leukoreduction, storage, and simulated transfusion for non‐LR and LR units. Immediately after leukoreduction, there was a significant increase in TXB 2 and PGF 2α concentrations, but during storage, these eicosanoids decreased to non‐LR concentrations. In both LR and non‐LR units, 6‐keto‐PGF 1α concentrations increased during storage and simulated transfusion, but there was no difference between unit type. There was no difference in AA, LTB 4, PGE 2, and PGD 2 concentrations between unit types.Conclusions and Clinical ImportanceLeukoreduction, storage, and simulated transfusion do not alter erythrocyte PS expression. Leukoreduction causes an immediate increase in concentrations of TXB 2 and PGF 2α, but concentrations decrease to non‐LR concentrations with storage. Leukoreduction does not decrease the accumulation of 6‐keto‐PGF 1α during storage.

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Section: Discussionmentioning

confidence: 99%

“…Although erythrocytes contain AA, they do not possess the oxidative enzymes involved in AA metabolism and eicosanoid synthesis 18. The leukocyte and platelet populations in units of pRBCs probably are the major contributors to AA metabolism 15.…”

mentioning

confidence: 99%

Effects of Leukoreduction and Storage on Erythrocyte Phosphatidylserine Expression and Eicosanoid Concentrations in Units of Canine Packed Red Blood Cells

Muro

Lee

Ross

et al. 2017

Veterinary Internal Medicne

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“…In contrast, blood platelets mainly produce TXA2. However, platelet PGH2 can be used by contiguous vascular endothelial cells to produce PGI2 via transcellular metabolism, and endothelial PGH2 can be converted by platelets or monocytes into TXA2 [10,11].…”

Section: Synthesis Of Prostanoids By Different Cell Typesmentioning

confidence: 99%

Prostanoids and NSAIDs in Cardiovascular Biology and Disease

Weksler

2015

Curr Atheroscler Rep

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Prostanoids and related arachidonic acid derivatives are important physiologic modulators in arteries, as well as mediators of inflammation, hemostasis, and cell proliferation. Their participation in atherosclerosis and in acute thrombotic events is complex, as demonstrated by untoward cardiovascular (CV) effects associated with clinical use of inhibitors of prostaglandin synthesis for treatment of chronic pain, inflammatory states, or cancer prophylaxis. Newer understanding of the pathophysiology of atherosclerosis and the pharmacology of prostanoids promises potential resolution of current problems resulting from the hazards of available prostanoid-altering drugs.

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“…In addition, n-3 DPA and n-6 DPA derived 7, 8, 17-trihydroxy-9, 11, 13, 15E, 19Z-docosapentaenoic acid RvD1 n-3 DPA , 7, 14-dihydroxy-8, 10, 12, 16Z, 19Z-docosapentaenoic acid MaR1 n-3 DPA , 17S -hydroxy-docosapentaenoic acid and 10,17S -dihydroxydocosapentaenoic acid have been identified as specialized pro-resolving mediators 20,21 . AA, which is a retro-conversion product of n-6 DPA, is an important fatty acid for cell membrane PLs, and is derived to eicosanoids, which perform physiological functions 22 . It is therefore important to investigate the metabolism of n-3 DPA and n-6 DPA to elucidate the molecular mechanisms of their beneficial health functions.…”

Section: Discussionmentioning

confidence: 99%