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Article: Regeneration of the endothelium in vascular injury

TitleRegeneration of the endothelium in vascular injury
Authors
KeywordsG-proteins
No
oxLDL
Regenerated endothelium
Issue Date2010
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0920-3206
Citation
Cardiovascular Drugs And Therapy, 2010, v. 24 n. 4, p. 299-303 How to Cite?
AbstractThe endothelium mediates relaxations (dilatations) of the underlying vascular smooth muscle cells. The endothelium-dependent relaxations are due to the release of non-prostanoid vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO). The endothelial cells also release substances (endothelium-derived hyperpolarizing factor, EDHF) that cause hyperpolarization of the cell membrane of the underlying vascular smooth muscle. The release of EDRF from the endothelium can be mediated by both pertussis toxin-sensitive Gi (alpha2-adrenergic activation, serotonin, thrombin) and insensitive Gq (adenosine diphosphate, bradykinin) coupling proteins. The ability of the endothelial cell to release relaxing factors can be upregulated by impregnation with estrogens, exercise and antioxidants, and down-regulated by oxidative stress and increased presence of oxidized LDL. Following injury or apoptotic death, the endothelium regenerates. However, in regenerated endothelial cells, there is an early selective loss of the pertussis-toxin sensitive mechanisms of EDRF-release. Functional studies suggest that abnormal handling of LDL because of increased oxidative stress play a key role in this selective loss. Genomic analysis demonstrates the emergence of fatty acid binding protein-A (A-FBP) and metalloproteinase-7 (MMP7) in regenerated endothelial cells. The reduced release of NO resulting from the endothelial dysfunction in regenerated areas creates a locus minoris resistentiae which favors the occurrence of vasospasm and thrombosis as well as the initiation of atherosclerosis. © Springer Science+Business Media, LLC 2010.
Persistent Identifierhttp://hdl.handle.net/10722/125252
ISSN
2015 Impact Factor: 3.189
2015 SCImago Journal Rankings: 1.114
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-10-31T11:20:08Z-
dc.date.available2010-10-31T11:20:08Z-
dc.date.issued2010en_HK
dc.identifier.citationCardiovascular Drugs And Therapy, 2010, v. 24 n. 4, p. 299-303en_HK
dc.identifier.issn0920-3206en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125252-
dc.description.abstractThe endothelium mediates relaxations (dilatations) of the underlying vascular smooth muscle cells. The endothelium-dependent relaxations are due to the release of non-prostanoid vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO). The endothelial cells also release substances (endothelium-derived hyperpolarizing factor, EDHF) that cause hyperpolarization of the cell membrane of the underlying vascular smooth muscle. The release of EDRF from the endothelium can be mediated by both pertussis toxin-sensitive Gi (alpha2-adrenergic activation, serotonin, thrombin) and insensitive Gq (adenosine diphosphate, bradykinin) coupling proteins. The ability of the endothelial cell to release relaxing factors can be upregulated by impregnation with estrogens, exercise and antioxidants, and down-regulated by oxidative stress and increased presence of oxidized LDL. Following injury or apoptotic death, the endothelium regenerates. However, in regenerated endothelial cells, there is an early selective loss of the pertussis-toxin sensitive mechanisms of EDRF-release. Functional studies suggest that abnormal handling of LDL because of increased oxidative stress play a key role in this selective loss. Genomic analysis demonstrates the emergence of fatty acid binding protein-A (A-FBP) and metalloproteinase-7 (MMP7) in regenerated endothelial cells. The reduced release of NO resulting from the endothelial dysfunction in regenerated areas creates a locus minoris resistentiae which favors the occurrence of vasospasm and thrombosis as well as the initiation of atherosclerosis. © Springer Science+Business Media, LLC 2010.en_HK
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0920-3206en_HK
dc.relation.ispartofCardiovascular Drugs and Therapyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThe original publication is available at www.springerlink.com-
dc.subjectG-proteinsen_HK
dc.subjectNoen_HK
dc.subjectoxLDLen_HK
dc.subjectRegenerated endotheliumen_HK
dc.subject.meshEndothelium, Vascular - pathology - physiology-
dc.subject.meshEndothelium-Dependent Relaxing Factors - physiology-
dc.subject.meshFatty Acid-Binding Proteins - physiology-
dc.subject.meshMatrix Metalloproteinase 7 - physiology-
dc.subject.meshNitric Oxide - physiology-
dc.titleRegeneration of the endothelium in vascular injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0920-3206&volume=24&issue=4&spage=299&epage=303&date=2010&atitle=Regeneration+of+the+endothelium+in+vascular+injury-
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1007/s10557-010-6257-5en_HK
dc.identifier.pmid20689986-
dc.identifier.scopuseid_2-s2.0-78149361257en_HK
dc.identifier.hkuros181434en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78149361257&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume24en_HK
dc.identifier.issue4en_HK
dc.identifier.spage299en_HK
dc.identifier.epage303en_HK
dc.identifier.isiWOS:000281978000002-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.citeulike7712913-

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