Trial reportFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
Inherited human group IVA cytosolic phospholipase A2 deficiency abolishes platelet, endothelial, and leucocyte eicosanoid generation.
Trial report in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Regulation of P450-derived epoxy fatty acids in cardiovascular diseases.Redox biochemistry and chemistry · 2025Article
- Characterization of Novel Variants inBiomolecules · 2025Article
- Defective CFTR modulates mechanosensitive channels TRPV4 and PIEZO1 and drives endothelial barrier failure.iScience · 2024Article
- Effects of sEH inhibition on the eicosanoid and cytokine storms in SARS-CoV-2-infected mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Renal Function Underpins the Cyclooxygenase-2: Asymmetric Dimethylarginine Axis in Mouse and Man.Kidney international reports · 2023Article
- Article
- Identification of a homozygous recessive variant inHaematologica · 2021Article
- Genetic Variants in Cytosolic Phospholipase A2 Associated With Nonsteroidal Anti-Inflammatory Drug-Induced Acute Urticaria/Angioedema.Frontiers in pharmacology · 2021Article
- Profiling the eicosanoid networks that underlie the anti- and pro-thrombotic effects of aspirin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Article
- Eicosanoids in platelets and the effect of their modulation by aspirin in the cardiovascular system (and beyond).British journal of pharmacology · 2019Review
- Eicosanoids, prostacyclin and cyclooxygenase in the cardiovascular system.British journal of pharmacology · 2019Review
- Kidney Transplantation in a Patient Lacking Cytosolic Phospholipase ACirculation research · 2018Article
- CD1a presentation of endogenous antigens by group 2 innate lymphoid cells.Science immunology · 2017Article
- 2-Oxoesters: A Novel Class of Potent and Selective Inhibitors of Cytosolic Group IVA Phospholipase AScientific reports · 2017Article
- Aspirin inhibits the production of proangiogenic 15(S)-HETE by platelet cyclooxygenase-1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Cytosolic phospholipase A2 contributes to innate immune defense against Candida albicans lung infection.BMC immunology · 2016Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
Eicosanoids are important vascular regulators, but the phospholipase A2 (PLA2) isoforms supporting their production within the cardiovascular system are not fully understood. To address this, we have studied platelets, endothelial cells, and leukocytes from 2 siblings with a homozygous loss-of-function mutation in group IVA cytosolic phospholipase A2 (cPLA2α). Chromatography/mass spectrometry was used to determine levels of a broad range of eicosanoids produced by isolated vascular cells, and in plasma and urine. Eicosanoid release data were paired with studies of cellular function. Absence of cPLA2α almost abolished eicosanoid synthesis in platelets (e.g., thromboxane A2, control 20.5 ± 1.4 ng/ml vs. patient 0.1 ng/ml) and leukocytes [e.g., prostaglandin E2 (PGE2), control 21.9 ± 7.4 ng/ml vs. patient 1.9 ng/ml], and this was associated with impaired platelet activation and enhanced inflammatory responses. cPLA2α-deficient endothelial cells showed reduced, but not absent, formation of prostaglandin I2 (prostacyclin; control 956 ± 422 pg/ml vs. patient 196 pg/ml) and were primed for inflammation. In the urine, prostaglandin metabolites were selectively influenced by cPLA2α deficiency. For example, prostacyclin metabolites were strongly reduced (18.4% of control) in patients lacking cPLA2α, whereas PGE2 metabolites (77.8% of control) were similar to healthy volunteer levels. These studies constitute a definitive account, demonstrating the fundamental role of cPLA2α to eicosanoid formation and cellular responses within the human circulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.