ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Mechanical induction of group V phospholipase A(2) causes lung inflammation and acute lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Bifidobacterium breve promotes growth and lipid alteration in Trichomonas vaginalis transiently through transcriptomic reprogramming.Scientific reports · 2026Article
- Alveolar macrophage-derived gVPLA2 promotes ventilator-induced lung injury via the cPLA2/PGE2 pathway.BMC pulmonary medicine · 2023Article
- Mechanotransduction Regulates the Interplays Between Alveolar Epithelial and Vascular Endothelial Cells in Lung.Frontiers in physiology · 2022Review
- Phospholipases A2 as biomarkers in acute respiratory distress syndrome.Biomedical journal · 2021Review
- Ventilator-induced lung-injury in mouse models: Is there a trap?Laboratory animal research · 2021Review
- Secretory Phospholipase ACell biochemistry and biophysics · 2021Review
- Group V Phospholipase ACells · 2021Article
- Degradation of group V secretory phospholipase AMicrovascular research · 2020Article
- Is Progression of Pulmonary Fibrosis due to Ventilation-induced Lung Injury?American journal of respiratory and critical care medicine · 2019Review
- Stromal-Interacting Molecule 1 (Stim1)/Orai1 Modulates Endothelial Permeability in Ventilator-Induced Lung Injury.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Sphingolipids in Ventilator Induced Lung Injury: Role of Sphingosine-1-Phosphate Lyase.International journal of molecular sciences · 2018Article
- Chronic high-magnitude cyclic stretch stimulates EC inflammatory response via VEGF receptor 2-dependent mechanism.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- The Roles of the Secreted Phospholipase AAdvances in immunology · 2016Review
- Group V Secretory Phospholipase A2 Is Involved in Tubular Integrity and Sodium Handling in the Kidney.PloS one · 2016Article
- A new era of secreted phospholipase A₂.Journal of lipid research · 2015Article
- Asef mediates HGF protective effects against LPS-induced lung injury and endothelial barrier dysfunction.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Asef controls vascular endothelial permeability and barrier recovery in the lung.Molecular biology of the cell · 2015Article
- Role of microtubules in attenuation of PepG-induced vascular endothelial dysfunction by atrial natriuretic peptide.Biochimica et biophysica acta · 2015Article
- Novel regulators of endothelial barrier function.American journal of physiology. Lung cellular and molecular physiology · 2014Review
- A critical review of the American Journal of Physiology-Lung Cellular and Molecular Physiology: 2012-2015.American journal of physiology. Lung cellular and molecular physiology · 2014Review
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6 authors at 3 institutions in 2 countries.
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Abstract
Ventilation at high tidal volume may cause lung inflammation and barrier dysfunction that culminates in ventilator-induced lung injury (VILI). However, the mechanisms by which mechanical stimulation triggers the inflammatory response have not been fully elucidated. This study tested the hypothesis that onset of VILI is triggered by activation of secretory group V phospholipase A(2) (gVPLA2) in pulmonary vascular endothelium exposed to excessive mechanical stretch. High-magnitude cyclic stretch (18% CS) increased expression and surface exposure of gVPLA2 in human pulmonary endothelial cells (EC). CS-induced gVPLA2 activation was required for activation of ICAM-1 expression and polymorphonuclear neutrophil (PMN) adhesion to CS-preconditioned EC. By contrast, physiological CS (5% CS) had no effect on gVPLA2 activation or EC-PMN adhesion. CS-induced ICAM-1 expression and EC-PMN adhesion were attenuated by the gVPLA2-blocking antibody (MCL-3G1), general inhibitor of soluble PLA2, LY311727, or siRNA-induced EC gVPLA2 knockdown. In vivo, ventilator-induced lung leukocyte recruitment, cell and protein accumulation in the alveolar space, and total lung myeloperoxidase activity were strongly suppressed in gVPLA2 mouse knockout model or upon administration of MCL-3G1. These results demonstrate a novel role for gVPLA2 as the downstream effector of pathological mechanical stretch leading to an inflammatory response associated with VILI.
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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.