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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

 

Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. China Medical University Shenyang
  3. China Medical University Hospital Taichung
  4. National Defense Medical Center Taiwan
  5. College of Life Sciences
  6. Taipei Medical University
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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