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Article: On the mechanism of the losartan-mediated inhibition of phosphatidylcholine biosynthesis in H9c2 cells

TitleOn the mechanism of the losartan-mediated inhibition of phosphatidylcholine biosynthesis in H9c2 cells
Authors
KeywordsAngiotensin II
Biosynthesis
Inhibition
Losartan
Phosphatidylcholine
Issue Date1997
PublisherElsevier BV.
Citation
Biochimica Et Biophysica Acta - Lipids And Lipid Metabolism, 1997, v. 1347 n. 2-3, p. 183-190 How to Cite?
AbstractPhosphatidylcholine is the major phospholipid in mammalian tissues and the biosynthesis of phosphatidylcholine in H9c2 cells was previously shown to be stimulated by angiotensin II. In this study, we used the potent AT1 receptor antagonist, losartan, to determine if the angiotensin II-mediated stimulation of phosphatidylcholine biosynthesis was mediated by AT1 receptors. H9c2 cells were incubated with angiotensin II in the absence or presence of various concentrations of losartan. The cells were then incubated with [methyl-3H]choline for an additional 60 min and the radioactivity incorporated into phosphatidylcholine and its choline-containing metabolites determined. Losartan at concentrations which block AT1 receptors did not effect phosphatidylcholine biosynthesis mediated by angiotensin II. In contrast, higher concentrations of losartan inhibited radioactivity incorporated into phosphatidylcholine and its metabolites and this was due to a losartan-mediated reduction in choline uptake. Kinetic studies revealed that the losartan-mediated inhibition of choline uptake was competitive. High concentrations of losartan caused a translocation of CTP:phosphocholine cytidylyltransferase from the cytosolic (inactive) to the membrane (active) fraction likely as a compensatory mechanism for the losartan-mediated reduction in new phosphatidylcholine biosynthesis. Incubation of cells with PD123319, a potent AT2-receptor antagonist, did not block the angiotensin II-mediated stimulation of phosphatidylcholine biosynthesis. The results suggest that angiotensin II stimulates phosphatidylcholine biosynthesis independent of AT1- and AT2-receptor activation and losartan inhibits phosphatidylcholine biosynthesis by reducing choline uptake in H9c2 cells.
Persistent Identifierhttp://hdl.handle.net/10722/80226
ISSN
2000 Impact Factor: 2.973
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHatch, GMen_HK
dc.contributor.authorLee, Den_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorKroeger, EAen_HK
dc.contributor.authorChoy, PCen_HK
dc.date.accessioned2010-09-06T08:03:56Z-
dc.date.available2010-09-06T08:03:56Z-
dc.date.issued1997en_HK
dc.identifier.citationBiochimica Et Biophysica Acta - Lipids And Lipid Metabolism, 1997, v. 1347 n. 2-3, p. 183-190en_HK
dc.identifier.issn0005-2760en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80226-
dc.description.abstractPhosphatidylcholine is the major phospholipid in mammalian tissues and the biosynthesis of phosphatidylcholine in H9c2 cells was previously shown to be stimulated by angiotensin II. In this study, we used the potent AT1 receptor antagonist, losartan, to determine if the angiotensin II-mediated stimulation of phosphatidylcholine biosynthesis was mediated by AT1 receptors. H9c2 cells were incubated with angiotensin II in the absence or presence of various concentrations of losartan. The cells were then incubated with [methyl-3H]choline for an additional 60 min and the radioactivity incorporated into phosphatidylcholine and its choline-containing metabolites determined. Losartan at concentrations which block AT1 receptors did not effect phosphatidylcholine biosynthesis mediated by angiotensin II. In contrast, higher concentrations of losartan inhibited radioactivity incorporated into phosphatidylcholine and its metabolites and this was due to a losartan-mediated reduction in choline uptake. Kinetic studies revealed that the losartan-mediated inhibition of choline uptake was competitive. High concentrations of losartan caused a translocation of CTP:phosphocholine cytidylyltransferase from the cytosolic (inactive) to the membrane (active) fraction likely as a compensatory mechanism for the losartan-mediated reduction in new phosphatidylcholine biosynthesis. Incubation of cells with PD123319, a potent AT2-receptor antagonist, did not block the angiotensin II-mediated stimulation of phosphatidylcholine biosynthesis. The results suggest that angiotensin II stimulates phosphatidylcholine biosynthesis independent of AT1- and AT2-receptor activation and losartan inhibits phosphatidylcholine biosynthesis by reducing choline uptake in H9c2 cells.en_HK
dc.languageengen_HK
dc.publisherElsevier BV.en_HK
dc.relation.ispartofBiochimica et Biophysica Acta - Lipids and Lipid Metabolismen_HK
dc.rightsBiochimica et Biophysica Acta. Copyright © Elsevier BV.en_HK
dc.subjectAngiotensin IIen_HK
dc.subjectBiosynthesisen_HK
dc.subjectInhibitionen_HK
dc.subjectLosartanen_HK
dc.subjectPhosphatidylcholineen_HK
dc.titleOn the mechanism of the losartan-mediated inhibition of phosphatidylcholine biosynthesis in H9c2 cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-3002&volume=1347&issue=2-3&spage=183&epage=190&date=1997&atitle=On+the+mechanism+of+the+losartan-mediated+inhibition+of+phosphatidylcholine+biosynthesis+in+H9c2+cellsen_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0005-2760(97)00062-3en_HK
dc.identifier.pmid9295162-
dc.identifier.scopuseid_2-s2.0-0031575186en_HK
dc.identifier.hkuros32774en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031575186&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1347en_HK
dc.identifier.issue2-3en_HK
dc.identifier.spage183en_HK
dc.identifier.epage190en_HK
dc.identifier.isiWOS:A1997XU60100007-
dc.identifier.scopusauthoridHatch, GM=7102271713en_HK
dc.identifier.scopusauthoridLee, D=7406668953en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.scopusauthoridKroeger, EA=7003400023en_HK
dc.identifier.scopusauthoridChoy, PC=7006633002en_HK

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