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Article: Propofol depresses angiotensin II-induced cell proliferation in rat cardiac fibroblasts

TitlePropofol depresses angiotensin II-induced cell proliferation in rat cardiac fibroblasts
Authors
Issue Date2010
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.org
Citation
Anesthesiology, 2010, v. 112 n. 1, p. 108-118 How to Cite?
Abstract
Background: Propofol may have beneficial effects on the prevention of angiotensin II (Ang II)-induced cardiac fibroblast proliferation via its antioxidative properties. The authors hypothesized that propofol may alter Ang II-induced cell proliferation and aimed to identify the putative underlying signaling pathways in rat cardiac fibroblasts. Methods: Cultured rat cardiac fibroblasts were pretreated with propofol then stimulated with Ang II; cell proliferation and endothelin-1 gene expression were examined. The effect of propofol on Ang II-induced nicotinamide adenine dinucleotide phosphate-oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, and activator protein 1-mediated reporter activity were also examined. The effect of propofol on nitric oxide production and protein kinase B and endothelial nitric oxide synthase phosphorylations were also tested to elucidate the intracellular mechanism of propofol in proliferation. Results: Ang II (100 nm) increased cell proliferation and endothelin-1 expression, which were partially inhibited by propofol (10 or 30 μm). Propofol also inhibited Ang II-increased nicotinamide adenine dinucleotide phosphate-oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, and activator protein 1-mediated reporter activity. Propofol was also found to increase nitric oxide generation and protein kinase B and nitric oxide synthase phosphorylations. Nitric oxide synthase inhibitor (N-nitro-l-arginine methylester) and the short interfering RNA transfection for protein kinase B or endothelial nitric oxide synthase markedly attenuated the inhibitory effect of propofol on Ang II-induced cell proliferation. Conclusions: The authors' Results suggest that propofol prevents cardiac fibroblast proliferation by interfering with the generation of reactive oxygen species and involves the activation of the protein kinase B-endothelial nitric oxide synthase-nitric oxide pathway. © 2010 American Society of Anesthesiologists, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/124468
ISSN
2013 Impact Factor: 6.168
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, THen_HK
dc.contributor.authorLeung, YMen_HK
dc.contributor.authorCheung, CWen_HK
dc.contributor.authorChen, CHen_HK
dc.contributor.authorChen, YLen_HK
dc.contributor.authorWong, KLen_HK
dc.date.accessioned2010-10-31T10:36:02Z-
dc.date.available2010-10-31T10:36:02Z-
dc.date.issued2010en_HK
dc.identifier.citationAnesthesiology, 2010, v. 112 n. 1, p. 108-118en_HK
dc.identifier.issn0003-3022en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124468-
dc.description.abstractBackground: Propofol may have beneficial effects on the prevention of angiotensin II (Ang II)-induced cardiac fibroblast proliferation via its antioxidative properties. The authors hypothesized that propofol may alter Ang II-induced cell proliferation and aimed to identify the putative underlying signaling pathways in rat cardiac fibroblasts. Methods: Cultured rat cardiac fibroblasts were pretreated with propofol then stimulated with Ang II; cell proliferation and endothelin-1 gene expression were examined. The effect of propofol on Ang II-induced nicotinamide adenine dinucleotide phosphate-oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, and activator protein 1-mediated reporter activity were also examined. The effect of propofol on nitric oxide production and protein kinase B and endothelial nitric oxide synthase phosphorylations were also tested to elucidate the intracellular mechanism of propofol in proliferation. Results: Ang II (100 nm) increased cell proliferation and endothelin-1 expression, which were partially inhibited by propofol (10 or 30 μm). Propofol also inhibited Ang II-increased nicotinamide adenine dinucleotide phosphate-oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, and activator protein 1-mediated reporter activity. Propofol was also found to increase nitric oxide generation and protein kinase B and nitric oxide synthase phosphorylations. Nitric oxide synthase inhibitor (N-nitro-l-arginine methylester) and the short interfering RNA transfection for protein kinase B or endothelial nitric oxide synthase markedly attenuated the inhibitory effect of propofol on Ang II-induced cell proliferation. Conclusions: The authors' Results suggest that propofol prevents cardiac fibroblast proliferation by interfering with the generation of reactive oxygen species and involves the activation of the protein kinase B-endothelial nitric oxide synthase-nitric oxide pathway. © 2010 American Society of Anesthesiologists, Inc.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.orgen_HK
dc.relation.ispartofAnesthesiologyen_HK
dc.subject.meshAnesthetics, Intravenous - pharmacologyen_HK
dc.subject.meshAngiotensin II - antagonists & inhibitors - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntimetabolites - diagnostic useen_HK
dc.subject.meshBlotting, Northernen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshBromodeoxyuridine - diagnostic useen_HK
dc.subject.meshCell Proliferation - drug effectsen_HK
dc.subject.meshCell Survival - drug effectsen_HK
dc.subject.meshDNA, Complementary - biosynthesis - geneticsen_HK
dc.subject.meshFibroblasts - drug effectsen_HK
dc.subject.meshFluoresceinsen_HK
dc.subject.meshMyocytes, Cardiac - drug effectsen_HK
dc.subject.meshNADPH Oxidase - metabolismen_HK
dc.subject.meshNitrates - metabolismen_HK
dc.subject.meshNitric Oxide Synthase - metabolismen_HK
dc.subject.meshNitrites - metabolismen_HK
dc.subject.meshOxidation-Reductionen_HK
dc.subject.meshPropofol - pharmacologyen_HK
dc.subject.meshRNA - biosynthesis - isolation & purificationen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshSuperoxides - metabolismen_HK
dc.subject.meshTransfectionen_HK
dc.titlePropofol depresses angiotensin II-induced cell proliferation in rat cardiac fibroblastsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0003-3022&volume=112&spage=108&epage=118&date=2010&atitle=Propofol+depresses+angiotensin+II-induced+cell+proliferation+in+rat+cardiac+fibroblastsen_HK
dc.identifier.emailCheung, CW:cheucw@hku.hken_HK
dc.identifier.authorityCheung, CW=rp00244en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1097/01.anes.0000365960.74268.21en_HK
dc.identifier.pmid20032702en_HK
dc.identifier.scopuseid_2-s2.0-74049119721en_HK
dc.identifier.hkuros175552en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-74049119721&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume112en_HK
dc.identifier.issue1en_HK
dc.identifier.spage108en_HK
dc.identifier.epage118en_HK
dc.identifier.isiWOS:000273314200018-
dc.publisher.placeUnited Statesen_HK

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