ArticleThe European respiratory journal2013
Iloprost improves endothelial barrier function in lipopolysaccharide-induced lung injury.
Article in The European respiratory journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- Extracellular Vesicles as Drivers of Lung Endothelial Dysfunction in ARDS: Mechanisms and Therapeutic Opportunities.Comprehensive Physiology · 2026Review
- NDRG1 aggravates Sepsis-Induced acute lung injury via PKM2-dependent activation of STAT3 and NF-κB signaling.BMC immunology · 2026Article
- Research hotspots and evolving trends of barrier dysfunction in acute lung injury and acute respiratory distress syndrome.Heliyon · 2024Article
- Designer high-density lipoprotein particles enhance endothelial barrier function and suppress inflammation.Science signaling · 2024Article
- Pulmonary drug delivery for acute respiratory distress syndrome.Pulmonary pharmacology & therapeutics · 2023Review
- 6'-Sialylactose abolished lipopolysaccharide-induced inflammation and hyper-permeability in endothelial cells.Archives of pharmacal research · 2022Article
- Induction of endothelial barrier dysfunction by serum factors in rats subjected to traumatic brain injury and hemorrhagic shock.Physiological reports · 2022Article
- The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19.International journal of molecular sciences · 2022Review
- Agonists for Bitter Taste Receptors T2R10 and T2R38 Attenuate LPS-Induced Permeability of the Pulmonary EndotheliumFrontiers in physiology · 2022Article
- Static Stretch Increases the Pro-Inflammatory Response of Rat Type 2 Alveolar Epithelial Cells to Dynamic Stretch.Frontiers in physiology · 2022Article
- Transcriptional Modulation of the Hippo Signaling Pathway by Drugs Used to Treat Bipolar Disorder and Schizophrenia.International journal of molecular sciences · 2021Article
- The modulatory role of sulfated and non-sulfated small molecule heparan sulfate-glycomimetics in endothelial dysfunction: absolute structural clarification, molecular docking and simulated dynamics, SAR analyses and ADMET studies.RSC medicinal chemistry · 2021Article
- Microtubule-dependent mechanism of anti-inflammatory effect of SOCS1 in endothelial dysfunction and lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Dissecting the Cellular Mechanism of Prostacyclin Analog Iloprost in Reversing Vascular Dysfunction in Scleroderma.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- Article
- Oxidized Phospholipids in Control of Endothelial Barrier Function: Mechanisms and Implication in Lung Injury.Frontiers in endocrinology · 2021Review
- Endothelial Dysfunction, Inflammation, and Oxidative Stress in COVID-19-Mechanisms and Therapeutic Targets.Oxidative medicine and cellular longevity · 2021Review
- Lipopolysaccharide-Induced Vascular Inflammation Model on Microfluidic Chip.Micromachines · 2020Article
- Phosphoproteome profiling provides insight into the mechanisms of ventilator-induced lung injury.Experimental and therapeutic medicine · 2020Article
- Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The protective effects of prostacyclin and its stable analogue iloprost are mediated by elevation of intracellular cyclic AMP (cAMP) leading to enhancement of the peripheral actin cytoskeleton and cell-cell adhesive structures. This study tested the hypothesis that iloprost may exhibit protective effects against lung injury and endothelial barrier dysfunction induced by bacterial wall lipopolysaccharide (LPS). Endothelial barrier dysfunction was assessed by measurements of transendothelial permeability, morphologically and by analysis of LPS-activated inflammatory signalling. In vivo, C57BL/6J mice were challenged with LPS with or without iloprost or 8-bromoadenosine-3',5'-cyclic monophosphate (Br-cAMP) treatment. Lung injury was monitored by measurements of bronchoalveolar lavage protein content, cell count and Evans blue extravasation. Iloprost and Br-cAMP attenuated the disruption of the endothelial monolayer, and suppressed the activation of p38 mitogen-activated protein kinase (MAPK), the nuclear factor (NF)-κB pathway, Rho signalling, intercellular adhesion molecular (ICAM)-1 expression and neutrophil migration after LPS challenge. In vivo, iloprost was effective against LPS-induced protein and neutrophil accumulation in bronchoalveolar lavage fluid, and reduced myeloperoxidase activation, ICAM-1 expression and Evans blue extravasation in the lungs. Inhibition of Rac activity abolished the barrier-protective and anti-inflammatory effects of iloprost and Br-cAMP. Iloprost-induced elevation of intracellular cAMP triggers Rac signalling, which attenuates LPS-induced NF-κB and p38 MAPK inflammatory pathways and the Rho-dependent mechanism of endothelial permeability.
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Registered trials
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