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dc.contributor.authorZemskov, Evgeny A.
dc.contributor.authorLucas, Rudolf
dc.contributor.authorVerin, Alexander D.
dc.contributor.authorUmapathy, Nagavedi S.
dc.date.accessioned2012-10-26T16:27:00Z
dc.date.available2012-10-26T16:27:00Z
dc.date.issued2011-01en_US
dc.identifier.citationJ Cardiovasc Dis Res. 2011 Jan-Mar; 2(1):14-22en_US
dc.identifier.issn0976-2833en_US
dc.identifier.pmid21716747en_US
dc.identifier.doi10.4103/0975-3583.78582en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/659
dc.description.abstractEndothelial cells (ECs), forming a semi-permeable barrier between the interior space of blood vessels and underlying tissues, control such diverse processes as vascular tone, homeostasis, adhesion of platelets, and leukocytes to the vascular wall and permeability of vascular wall for cells and fluids. Mechanisms which govern the highly clinically relevant process of increased EC permeability are under intense investigation. It is well known that loss of this barrier (permeability increase) results in tissue inflammation, the hall mark of inflammatory diseases such as acute lung injury and its severe form, acute respiratory distress syndrome. Little is known about processes which determine the endothelial barrier enhancement or protection against permeability increase. It is now well accepted that extracellular purines and pyrimidines are promising and physiologically relevant barrier-protective agents and their effects are mediated by interaction with cell surface P2Y receptors which belong to the superfamily of G-protein-coupled receptors. The therapeutic potential of P2Y receptors is rapidly expanding field in pharmacology and some selective agonists became recently available. Here, we present an overview of recently identified P2Y receptor agonists that enhance the pulmonary endothelial barrier and inhibit and/or reverse endothelial barrier disruption.
dc.rightsCopyright: © Journal of Cardiovascular Disease Researchen_US
dc.subjectInvited Reviewen_US
dc.titleP2Y receptors as regulators of lung endothelial barrier integrityen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3120267en_US
dc.contributor.corporatenameVascular Biology Center
dc.contributor.corporatenameDepartment of Pulmonary and Critical Care
refterms.dateFOA2019-04-10T00:28:43Z
html.description.abstractEndothelial cells (ECs), forming a semi-permeable barrier between the interior space of blood vessels and underlying tissues, control such diverse processes as vascular tone, homeostasis, adhesion of platelets, and leukocytes to the vascular wall and permeability of vascular wall for cells and fluids. Mechanisms which govern the highly clinically relevant process of increased EC permeability are under intense investigation. It is well known that loss of this barrier (permeability increase) results in tissue inflammation, the hall mark of inflammatory diseases such as acute lung injury and its severe form, acute respiratory distress syndrome. Little is known about processes which determine the endothelial barrier enhancement or protection against permeability increase. It is now well accepted that extracellular purines and pyrimidines are promising and physiologically relevant barrier-protective agents and their effects are mediated by interaction with cell surface P2Y receptors which belong to the superfamily of G-protein-coupled receptors. The therapeutic potential of P2Y receptors is rapidly expanding field in pharmacology and some selective agonists became recently available. Here, we present an overview of recently identified P2Y receptor agonists that enhance the pulmonary endothelial barrier and inhibit and/or reverse endothelial barrier disruption.


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