ArticleThe Journal of clinical investigation1999
Platelet-activating factor mediates acid-induced lung injury in genetically engineered mice.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 125 citations in OpenAlex.
- Article
- Advances in research on the effects of platelet activation in acute lung injury (Review).Biomedical reports · 2022Review
- Association of platelet-activating factor receptor gene rs5938 (G/T) and rs313152 (T/C) polymorphisms with coronary heart disease and blood stasis syndrome in a Chinese Han population.Chinese journal of integrative medicine · 2017Article
- Biosynthesis of oxidized lipid mediators via lipoprotein-associated phospholipase A2 hydrolysis of extracellular cardiolipin induces endothelial toxicity.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Article
- To hydrolyze or not to hydrolyze: the dilemma of platelet-activating factor acetylhydrolase.Journal of lipid research · 2014Review
- Platelets induce endothelial tissue factor expression in a mouse model of acid-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Constructing the Architecturally Distinctive ABD-Tricycle of Phomactin A through an IntramolecularTetrahedron · 2011Article
- Total synthesis of (±)-phomactin A. Lessons learned from respecting a challenging structural topology.The Journal of organic chemistry · 2011Article
- Do soluble mediators cause ventilator-induced lung injury and multi-organ failure?Intensive care medicine · 2010Review
- Common pathways for activation of proinflammatory gene expression by G protein-coupled receptors in primary lung epithelial and endothelial cells.Experimental lung research · 2009Article
- Role of protease activated receptor 2 in experimental acute lung injury and lung fibrosis.Anatomical record (Hoboken, N.J. : 2007) · 2009Article
- The role of platelets in acute lung injury (ALI).Frontiers in bioscience (Landmark edition) · 2009Review
- Therapeutic inhibition of CXCR2 by Reparixin attenuates acute lung injury in mice.British journal of pharmacology · 2008Article
- Attenuation of folic acid-induced renal inflammatory injury in platelet-activating factor receptor-deficient mice.The American journal of pathology · 2006Article
- Cytosolic phospholipase A2-alpha is necessary for platelet-activating factor biosynthesis, efficient neutrophil-mediated bacterial killing, and the innate immune response to pulmonary infection: cPLA2-alpha does not regulate neutrophil NADPH oxidase activity.The Journal of biological chemistry · 2005Article
- Role of PAF receptors during intestinal ischemia and reperfusion injury. A comparative study between PAF receptor-deficient mice and PAF receptor antagonist treatment.British journal of pharmacology · 2003Article
- Role of the platelet-activating factor (PAF) receptor during pulmonary infection with gram negative bacteria.British journal of pharmacology · 2002Article
- Effects of the PAF receptor antagonist UK74505 on local and remote reperfusion injuries following ischaemia of the superior mesenteric artery in the rat.British journal of pharmacology · 2000Article
- Two of the usual suspects, platelet-activating factor and its receptor, implicated in acute lung injury.The Journal of clinical investigation · 1999Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adult respiratory distress syndrome (ARDS) is an acute lung injury of high mortality rate, and the molecular mechanisms underlying it are poorly understood. Acid aspiration-induced lung injury is one of the most common causes of ARDS, characterized by an increase in lung permeability, enhanced polymorphonuclear neutrophil (PMN) sequestration, and respiratory failure. Here, we investigated the role of platelet-activating factor (PAF) and the PAF receptor (PAFR) gene in a murine model of acid aspiration-induced lung injury. Overexpression of the PAFR gene in transgenic mice enhanced lung injury, pulmonary edema, and deterioration of gas exchange caused by HCl aspiration. Conversely, mice carrying a targeted disruption of the PAFR gene experienced significantly less acid-induced injury, edema, and respiratory failure. Nevertheless, the efficiency of PMN sequestration in response to acid aspiration was unaffected by differences in PAFR expression level. The current observations suggest that PAF is involved in the pathogenesis of acute lung injury caused by acid aspiration. Thus, inhibition of this pathway might provide a novel therapeutic approach to acute lung injury, for which no specific pharmaceutical agents are currently available.
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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.