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Conference Paper: Expressions of Urotensin II and Urotensin II Receptor are Up-regulated in Cardiovascular Tissues in Experimentally Induced Endotoxaemia

TitleExpressions of Urotensin II and Urotensin II Receptor are Up-regulated in Cardiovascular Tissues in Experimentally Induced Endotoxaemia
Authors
KeywordsInflammation
Urotensin II
Urotensin II Receptor
Issue Date2005
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/amjhyper
Citation
American Journal of Hypertension, 2005, v. 18 n. S4, p. 125A How to Cite?
AbstractUrotensin II (UII) is a cyclic, vasoactive neuropeptide identified as the ligand for a novel G-protein coupled receptor, referred to as the UT-II receptor (UT-IIR). Recent studies have indicated that cardiovascular effects of UII are mediated by its receptor, UT-IIR. UII promotes hypertrophy of cardiac myocytes, and its expression is up-regulated in infarcted rat heart and in congestive heart failure in humans. Expression of UT-IIR is low to undetectable in the healthy myocardium, but is up-regulated in the ischemic and post-infarct myocardium. The expression of UT is increased by interferon-gamma, suggesting a possible up-regulation of UII and UT-IIR as a consequence of an inflammatory response, which may lead to adverse cardiac remodeling. Accordingly, we examined the expression and localization of UII and its receptor in the cardiovascular tissues of rat after treatment with lipopolysaccharide (LPS) endotoxin. Male Sprague-Dawley rats were sacrificed at 1 hr after intra-peritoneal injection of LPS at 10 mg/kg weight, or saline as control. Cardiovascular tissues were dissected out and homogenized, and the expression of UII and UT-IIR mRNA was determined by RT-PCR. We found that UT-IIR expression was markedly increased by LPS in the left and right atria, thoracic artery and mesenteric artery (MA), but not in the left and right ventricles where high basal levels of UT-IIR expression were observed even without LPS stimulation. On the other hand, UII expression was significantly increased by LPS in almost all of the cardiovascular tissues tested, except in MA where there was no significant UII expression in both the control and LPS-treated animals. In conclusion, our results show that the expression of UII and UT-IIR receptor in cardiac tissues is up-regulated in inflammatory conditions and this might contribute to myocardial dysfunction in septic shock.
Persistent Identifierhttp://hdl.handle.net/10722/104999
ISSN
2015 Impact Factor: 3.182
2015 SCImago Journal Rankings: 1.397

 

DC FieldValueLanguage
dc.contributor.authorWong, LYFen_HK
dc.contributor.authorCheung, BMYen_HK
dc.contributor.authorLi, YYen_HK
dc.contributor.authorTang, F-
dc.date.accessioned2010-09-25T22:16:07Z-
dc.date.available2010-09-25T22:16:07Z-
dc.date.issued2005en_HK
dc.identifier.citationAmerican Journal of Hypertension, 2005, v. 18 n. S4, p. 125Aen_HK
dc.identifier.issn0895-7061en_HK
dc.identifier.urihttp://hdl.handle.net/10722/104999-
dc.description.abstractUrotensin II (UII) is a cyclic, vasoactive neuropeptide identified as the ligand for a novel G-protein coupled receptor, referred to as the UT-II receptor (UT-IIR). Recent studies have indicated that cardiovascular effects of UII are mediated by its receptor, UT-IIR. UII promotes hypertrophy of cardiac myocytes, and its expression is up-regulated in infarcted rat heart and in congestive heart failure in humans. Expression of UT-IIR is low to undetectable in the healthy myocardium, but is up-regulated in the ischemic and post-infarct myocardium. The expression of UT is increased by interferon-gamma, suggesting a possible up-regulation of UII and UT-IIR as a consequence of an inflammatory response, which may lead to adverse cardiac remodeling. Accordingly, we examined the expression and localization of UII and its receptor in the cardiovascular tissues of rat after treatment with lipopolysaccharide (LPS) endotoxin. Male Sprague-Dawley rats were sacrificed at 1 hr after intra-peritoneal injection of LPS at 10 mg/kg weight, or saline as control. Cardiovascular tissues were dissected out and homogenized, and the expression of UII and UT-IIR mRNA was determined by RT-PCR. We found that UT-IIR expression was markedly increased by LPS in the left and right atria, thoracic artery and mesenteric artery (MA), but not in the left and right ventricles where high basal levels of UT-IIR expression were observed even without LPS stimulation. On the other hand, UII expression was significantly increased by LPS in almost all of the cardiovascular tissues tested, except in MA where there was no significant UII expression in both the control and LPS-treated animals. In conclusion, our results show that the expression of UII and UT-IIR receptor in cardiac tissues is up-regulated in inflammatory conditions and this might contribute to myocardial dysfunction in septic shock.-
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/amjhyperen_HK
dc.relation.ispartofAmerican Journal of Hypertensionen_HK
dc.rightsAmerican Journal of hypertension. Copyright © Elsevier Inc.en_HK
dc.subjectInflammation-
dc.subjectUrotensin II-
dc.subjectUrotensin II Receptor-
dc.titleExpressions of Urotensin II and Urotensin II Receptor are Up-regulated in Cardiovascular Tissues in Experimentally Induced Endotoxaemiaen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0895-7061&volume=18&spage=125A&epage=&date=2005&atitle=Expressions+of+Urotensin+II+and+Urotensin+II+Receptor+are+Up-regulated+in+Cardiovascular+Tissues+in+Experimentally+Induced+Endotoxaemiaen_HK
dc.identifier.emailCheung, BMY: mycheung@hku.hken_HK
dc.identifier.emailTang, F: ftang@hkucc.hku.hken_HK
dc.identifier.authorityTang, F=rp00327en_HK
dc.identifier.doi10.1016/j.amjhyper.2005.03.348-
dc.identifier.hkuros105088en_HK
dc.identifier.volume18en_HK
dc.identifier.issueS4-
dc.identifier.spage125en_HK

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