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
2011 Impact Factor: 5.359
2011 SCImago Journal Rankings: 0.266
DOIhttp://dx.doi.org/10.1097/01.anes.0000365960.74268.21
ISI Accession Number IDWOS:000273314200018
ReferencesReferences in Scopus
DC Field
Value
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_subscribed_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
2011 Impact Factor: 5.359
2011 SCImago Journal Rankings: 0.266
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
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