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Article: Cellular signaling and NO production

TitleCellular signaling and NO production
Authors
KeywordsCaveola
Diabetes
Endothelium-derived relaxing factor (EDRF)
G-proteins
Hypertension
Nitric oxide
Nitric oxide synthase
Phosphorylation
Issue Date2010
PublisherSpringer. The Journal's web site is located at http://link.springer.de/link/service/journals/00424/index.htm
Citation
Pflugers Archiv European Journal Of Physiology, 2010, v. 459 n. 6, p. 807-816 How to Cite?
AbstractThe endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances. The best characterized endothelium-derived relaxing factor is nitric oxide (NO), which is synthesized by the endothelial isoform of nitric oxide synthase (eNOS). Endothelium-dependent relaxations involve both pertussis-toxin-sensitive G i (e.g., responses to serotonin, sphingosine 1-phosphate, alpha 2-adrenergic agonists, and thrombin) and pertussis-toxin-insensitive Gq (e.g., adenosine diphosphate and bradykinin) coupling proteins. eNOS undergoes a complex pattern of intracellular regulation, including post-translational modifications involving enzyme acylation and phosphorylation. eNOS is reversibly targeted to signal-transducing plasmalemmal caveolae where the enzyme interacts with a number of regulatory proteins, many of which are modified in cardiovascular disease states. The release of nitric oxide by the endothelial cell can be up- (e.g., by estrogens, exercise, and dietary factors) and down-regulated (e.g. oxidative stress, smoking, and oxidized low-density lipoproteins). It is reduced in the course of vascular disease (e.g., diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively lose the pertussis-toxin-sensitive pathway for NO release which favors vasospasm, thrombosis, penetration of macrophages, cellular growth, and the inflammatory reaction leading to atherosclerosis. The unraveling of the complex interaction of the pathways regulating the presence and the activity of eNOS will enhance the understanding of the perturbations in endothelium-dependent signaling that are seen in cardiovascular disease states, and may lead to the identification of novel targets for therapeutic intervention. © 2010 Springer-Verlag.
Persistent Identifierhttp://hdl.handle.net/10722/80307
ISSN
2015 Impact Factor: 3.654
2015 SCImago Journal Rankings: 1.638
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMichel, Ten_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-06T08:04:51Z-
dc.date.available2010-09-06T08:04:51Z-
dc.date.issued2010en_HK
dc.identifier.citationPflugers Archiv European Journal Of Physiology, 2010, v. 459 n. 6, p. 807-816en_HK
dc.identifier.issn0031-6768en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80307-
dc.description.abstractThe endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances. The best characterized endothelium-derived relaxing factor is nitric oxide (NO), which is synthesized by the endothelial isoform of nitric oxide synthase (eNOS). Endothelium-dependent relaxations involve both pertussis-toxin-sensitive G i (e.g., responses to serotonin, sphingosine 1-phosphate, alpha 2-adrenergic agonists, and thrombin) and pertussis-toxin-insensitive Gq (e.g., adenosine diphosphate and bradykinin) coupling proteins. eNOS undergoes a complex pattern of intracellular regulation, including post-translational modifications involving enzyme acylation and phosphorylation. eNOS is reversibly targeted to signal-transducing plasmalemmal caveolae where the enzyme interacts with a number of regulatory proteins, many of which are modified in cardiovascular disease states. The release of nitric oxide by the endothelial cell can be up- (e.g., by estrogens, exercise, and dietary factors) and down-regulated (e.g. oxidative stress, smoking, and oxidized low-density lipoproteins). It is reduced in the course of vascular disease (e.g., diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively lose the pertussis-toxin-sensitive pathway for NO release which favors vasospasm, thrombosis, penetration of macrophages, cellular growth, and the inflammatory reaction leading to atherosclerosis. The unraveling of the complex interaction of the pathways regulating the presence and the activity of eNOS will enhance the understanding of the perturbations in endothelium-dependent signaling that are seen in cardiovascular disease states, and may lead to the identification of novel targets for therapeutic intervention. © 2010 Springer-Verlag.en_HK
dc.languageengen_HK
dc.publisherSpringer. The Journal's web site is located at http://link.springer.de/link/service/journals/00424/index.htmen_HK
dc.relation.ispartofPflugers Archiv European Journal of Physiologyen_HK
dc.rightsThe original publication is available at www.springerlink.com-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCaveolaen_HK
dc.subjectDiabetesen_HK
dc.subjectEndothelium-derived relaxing factor (EDRF)en_HK
dc.subjectG-proteinsen_HK
dc.subjectHypertensionen_HK
dc.subjectNitric oxideen_HK
dc.subjectNitric oxide synthaseen_HK
dc.subjectPhosphorylationen_HK
dc.subject.meshEndothelium, Vascular - drug effects - physiology-
dc.subject.meshNitric Oxide - physiology-
dc.subject.meshNitric Oxide Synthase Type III - metabolism-
dc.subject.meshPhosphorylation-
dc.subject.meshSignal Transduction-
dc.titleCellular signaling and NO productionen_HK
dc.typeArticleen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1007/s00424-009-0765-9en_HK
dc.identifier.pmid20082095-
dc.identifier.scopuseid_2-s2.0-77952891006en_HK
dc.identifier.hkuros170216en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77952891006&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume459en_HK
dc.identifier.issue6en_HK
dc.identifier.spage807en_HK
dc.identifier.epage816en_HK
dc.identifier.isiWOS:000277376200004-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridMichel, T=7102599672en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.citeulike6803427-

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