ArticleThe Journal of clinical investigation1993
Role of phosphodiesterases in the regulation of endothelial permeability in vitro.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 187 citations in OpenAlex.
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- Defining the vascular niche of human adipose tissue across metabolic states.bioRxiv : the preprint server for biology · 2025Article
- Genetic and Inflammatory Signatures Associated With Worse Prognosis in Hospitalized Patients With Severe SARS-CoV-2 Infection With and Without Diabetes.Journal of medical virology · 2025Article
- Bioengineered 3D microvessels and complementary animal models reveal mechanisms of Trypanosoma congolense sequestration.Communications biology · 2025Article
- The effects of sepsis on endothelium and clinical implications.Cardiovascular research · 2021Article
- Evaluation of Real-Life Investigational Use of Enoximone in Asthma, the Third Step in Drug Repurposing: A Preliminary Report.Canadian respiratory journal · 2021Article
- Rho and Reactive Oxygen Species at Crossroads of Endothelial Permeability and Inflammation.Antioxidants & redox signaling · 2019Article
- Intracellular ascorbate tightens the endothelial permeability barrier through Epac1 and the tubulin cytoskeleton.American journal of physiology. Cell physiology · 2016Article
- Reinforcing endothelial junctions prevents microvessel permeability increase and tumor cell adhesion in microvessels in vivo.Scientific reports · 2015Article
- Role of cAMP-dependent protein kinase A activity in low-dose endothelial monocyte-activating polypeptide-II-induced opening of blood-tumor barrier.Journal of molecular neuroscience : MN · 2015Article
- Temporal effects of vascular endothelial growth factor and 3,5-cyclic monophosphate on blood-brain barrier solute permeability in vivo.Journal of neuroscience research · 2014Article
- Dynamics of pulmonary endothelial barrier function in acute inflammation: mechanisms and therapeutic perspectives.Cell and tissue research · 2014Review
- The Effect of Stress-Induced Senescence on Aging Human Cord Blood-Derived Endothelial Cells.Cardiovascular engineering and technology · 2013Article
- Phosphodiesterase 4 inhibition attenuates plasma volume loss and transvascular exchange in volume-expanded mice.The Journal of physiology · 2012Article
- Phosphodiesterase 4 inhibition attenuates atrial natriuretic peptide-induced vascular hyperpermeability and loss of plasma volume.The Journal of physiology · 2011Article
- Regulation of endothelial barrier function by cyclic nucleotides: the role of phosphodiesterases.Handbook of experimental pharmacology · 2011Review
- Mitigation of chlorine lung injury by increasing cyclic AMP levels.Proceedings of the American Thoracic Society · 2010Review
- Development and validation of a transcreener assay for detection of AMP- and GMP-producing enzymes.Assay and drug development technologies · 2010Article
- Dual PDE3/4 inhibitors as therapeutic agents for chronic obstructive pulmonary disease.British journal of pharmacology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophil-derived hydrogen peroxide (H2O2) is believed to play an important role in the pathogenesis of vascular injury and pulmonary edema. H2O2 time- and dose-dependently increased the hydraulic conductivity and decreased the selectivity of an endothelial cell monolayer derived from porcine pulmonary arteries. Effects of H2O2 on endothelial permeability were completely inhibited by adenylate cyclase activation with 10(-12) M cholera toxin or 0.1 microM forskolin. 10(-8) M Sp-cAMPS, a cAMP-dependent protein kinase A agonist, was similarly effective. The phosphodiesterase (PDE) inhibitors motapizone (10(-4) M), rolipram (10(-6) M), and zardaverine (10(-8) M), which specifically inhibit PDE-isoenzymes III, IV, and III/IV potently blocked H2O2-induced endothelial permeability when combined with 10(-6) M prostaglandin E1. Overall cellular cAMP content and inhibition of H2O2 effects on endothelial permeability were poorly correlated. H2O2 exposure resulted in a rapid and substantial decrease in endothelial cAMP content. The analysis of the PDE isoenzyme spectrum showed high activities of isoenzymes II, III, and IV in porcine pulmonary endothelial cells. The data suggest that adenylate cyclase activation/PDE inhibition is a powerful approach to block H2O2-induced increase in endothelial permeability. This concept appears especially valuable when endothelial PDE isoenzyme pattern and PDE inhibitor profile are matched optimally.
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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.