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Article: Propofol depresses angiotensin II-induced cell proliferation in rat cardiac fibroblasts
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TitlePropofol depresses angiotensin II-induced cell proliferation in rat cardiac fibroblasts
 
AuthorsCheng, TH5
Leung, YM2
Cheung, CW1
Chen, CH6
Chen, YL4
Wong, KL3
 
Issue Date2010
 
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.org
 
CitationAnesthesiology, 2010, v. 112 n. 1, p. 108-118 [How to Cite?]
DOI: http://dx.doi.org/10.1097/01.anes.0000365960.74268.21
 
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.
 
ISSN0003-3022
2013 Impact Factor: 6.168
 
DOIhttp://dx.doi.org/10.1097/01.anes.0000365960.74268.21
 
ISI Accession Number IDWOS:000273314200018
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorCheng, TH
 
dc.contributor.authorLeung, YM
 
dc.contributor.authorCheung, CW
 
dc.contributor.authorChen, CH
 
dc.contributor.authorChen, YL
 
dc.contributor.authorWong, KL
 
dc.date.accessioned2010-10-31T10:36:02Z
 
dc.date.available2010-10-31T10:36:02Z
 
dc.date.issued2010
 
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.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationAnesthesiology, 2010, v. 112 n. 1, p. 108-118 [How to Cite?]
DOI: http://dx.doi.org/10.1097/01.anes.0000365960.74268.21
 
dc.identifier.doihttp://dx.doi.org/10.1097/01.anes.0000365960.74268.21
 
dc.identifier.epage118
 
dc.identifier.hkuros175552
 
dc.identifier.isiWOS:000273314200018
 
dc.identifier.issn0003-3022
2013 Impact Factor: 6.168
 
dc.identifier.issue1
 
dc.identifier.openurl
 
dc.identifier.pmid20032702
 
dc.identifier.scopuseid_2-s2.0-74049119721
 
dc.identifier.spage108
 
dc.identifier.urihttp://hdl.handle.net/10722/124468
 
dc.identifier.volume112
 
dc.languageeng
 
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofAnesthesiology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnesthetics, Intravenous - pharmacology
 
dc.subject.meshAngiotensin II - antagonists & inhibitors - pharmacology
 
dc.subject.meshAnimals
 
dc.subject.meshAntimetabolites - diagnostic use
 
dc.subject.meshBlotting, Northern
 
dc.subject.meshBlotting, Western
 
dc.subject.meshBromodeoxyuridine - diagnostic use
 
dc.subject.meshCell Proliferation - drug effects
 
dc.subject.meshCell Survival - drug effects
 
dc.subject.meshDNA, Complementary - biosynthesis - genetics
 
dc.subject.meshFibroblasts - drug effects
 
dc.subject.meshFluoresceins
 
dc.subject.meshMyocytes, Cardiac - drug effects
 
dc.subject.meshNADPH Oxidase - metabolism
 
dc.subject.meshNitrates - metabolism
 
dc.subject.meshNitric Oxide Synthase - metabolism
 
dc.subject.meshNitrites - metabolism
 
dc.subject.meshOxidation-Reduction
 
dc.subject.meshPropofol - pharmacology
 
dc.subject.meshRNA - biosynthesis - isolation & purification
 
dc.subject.meshRats
 
dc.subject.meshRats, Sprague-Dawley
 
dc.subject.meshSuperoxides - metabolism
 
dc.subject.meshTransfection
 
dc.titlePropofol depresses angiotensin II-induced cell proliferation in rat cardiac fibroblasts
 
dc.typeArticle
 
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<contributor.author>Leung, YM</contributor.author>
<contributor.author>Cheung, CW</contributor.author>
<contributor.author>Chen, CH</contributor.author>
<contributor.author>Chen, YL</contributor.author>
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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