ArticleBiochemistry2010
Endothelial cell prostaglandin I(2) and platelet-activating factor production are markedly attenuated in the calcium-independent phospholipase A(2)beta knockout mouse.
Article in Biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Inherited human group IVA cytosolic phospholipase A2 deficiency abolishes platelet, endothelial, and leucocyte eicosanoid generation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Trial
- Anticoagulant and signaling functions of antithrombin.Journal of thrombosis and haemostasis : JTH · 2020Review
- iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Eicosanoids, prostacyclin and cyclooxygenase in the cardiovascular system.British journal of pharmacology · 2019Review
- Cigarette smoking promotes bladder cancer via increased platelet-activating factor.Physiological reports · 2019Article
- Cigarette smoke-induced urothelial cell damage: potential role of platelet-activating factor.Physiological reports · 2017Article
- Increased susceptibility to bladder inflammation in smokers: targeting the PAF-PAF receptor interaction to manage inflammatory cell recruitment.Physiological reports · 2015Article
- Enhanced breast cancer cell adherence to the lung endothelium via PAF acetylhydrolase inhibition: a potential mechanism for enhanced metastasis in smokers.American journal of physiology. Cell physiology · 2014Article
- Upregulated expression of brain enzymatic markers of arachidonic and docosahexaenoic acid metabolism in a rat model of the metabolic syndrome.BMC neuroscience · 2012Article
- Disturbed brain phospholipid and docosahexaenoic acid metabolism in calcium-independent phospholipase A(2)-VIA (iPLA(2)β)-knockout mice.Biochimica et biophysica acta · 2012Article
- Molecular mechanisms regulating the vascular prostacyclin pathways and their adaptation during pregnancy and in the newborn.Pharmacological reviews · 2012Review
- Sexual dimorphism in endothelin-1 induced mechanical hyperalgesia in the rat.Experimental neurology · 2012Article
- Lung endothelial cell platelet-activating factor production and inflammatory cell adherence are increased in response to cigarette smoke component exposure.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Analysis of two major intracellular phospholipases A(2) (PLA(2)) in mast cells reveals crucial contribution of cytosolic PLA(2)α, not Ca(2+)-independent PLA(2)β, to lipid mobilization in proximal mast cells and distal fibroblasts.The Journal of biological chemistry · 2011Article
- Platelet-activating factor and metastasis: calcium-independent phospholipase A2β deficiency protects against breast cancer metastasis to the lung.American journal of physiology. Cell physiology · 2011Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Damage and activation of lung endothelium can lead to interstitial edema, infiltration of inflammatory cells into the interstitium and airways, and production of inflammatory metabolites, all of which propagate airway inflammation in a variety of diseases. We have previously determined that stimulation of human microvascular endothelial cells from lung (HMVEC-L) results in activation of a calcium-independent phospholipase A(2) (iPLA(2)), and this leads to arachidonic acid release and production of prostaglandin I(2) (PGI(2)) and platelet-activating factor (PAF). We stimulated lung endothelial cells isolated from iPLA(2)beta-knockout (KO) and wild type (WT) mice with thrombin and tryptase to determine the role of iPLA(2)beta in endothelial cell membrane phospholipid hydrolysis. Thrombin or tryptase stimulation of WT lung endothelial cells resulted in increased arachidonic acid release and production of PGI(2) and PAF. Arachidonic acid release and PGI(2) production by stimulated iPLA(2)beta-KO endothelial cells were significantly reduced compared to WT. Measured PLA(2) activity and PGI(2) production by iPLA(2)beta-KO cells were suppressed by pretreatment with (R)-bromoenol lactone (R-BEL), which is a selective inhibitor of iPLA2gamma. In contrast to the increase in PAF production induced by stimulation of WT endothelial cells, none was observed for KO cells, and this suggests that endothelial PAF production is entirely dependent on iPLA(2)beta activity. Because inflammatory cell recruitment involves the interaction of endothelial cell PAF with PAF receptors on circulating cells, these data suggest that iPLA(2)beta may be a suitable therapeutic target for the treatment of inflammatory lung diseases.
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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.