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Article: Nitric oxide down-regulates caveolin-1 expression in rat brains during focal cerebral ischemia and reperfusion injury

TitleNitric oxide down-regulates caveolin-1 expression in rat brains during focal cerebral ischemia and reperfusion injury
Authors
KeywordsCaveolin-1
Ischemic stroke
Nitric oxide
Nitric oxide synthase
Issue Date2006
PublisherBlackwell Publishing Ltd.
Citation
Journal Of Neurochemistry, 2006, v. 96 n. 4, p. 1078-1089 How to Cite?
AbstractAs a signalling molecule of the integral membrane protein family, caveolin participates in cellular signal transduction via interaction with other signalling molecules. The nature of interaction between nitric oxide (NO) and caveolin in the brain, however, remains largely unknown. In this study we investigated the role(s) of NO in regulating caveolin-1 expression in rat ischemic brains with middle cerebral artery occlusion (MCAO). Exposure to 1 h ischemia induced the increases in neuronal nitric oxide synthase (nNOS) and NO concentration with concurrent down-regulation of caveolin-1 expression in the ischemic core of rat brains. Subsequent 24 h or more reperfusion time led to an increase in inducible NOS (iNOS) expression and NO production, as well as a decline of caveolin-1 protein at the core and penumbra of the ischemic brain. Afterwards, NOS inhibitors and an NO donor were utilized to clarify the link between NO production and caveolin-1 expression in the rats with 1 h ischemia plus 24 h reperfusion. NG-nitro-l-arginine methyl ester (L-NAME, a non-selective NOS inhibitor), N6-(1-iminoethyl)-lysine (NIL, an iNOS inhibitor), and 7-nitroindazole (7-NI, a nNOS inhibitor) prevented the loss of caveolin-1 in the core and penumbra of the ischemic brain, whereas l-N 5-(1-iminoethyl)-ornithine (L-NIO, an endothelial NOS inhibitor) showed less effect than the other NOS inhibitors. S-Nitroso-N- acetylpenicillamine (SNAP, a NO donor) down-regulated the expression of caveolin-1 protein in normal and ischemic brains. These results, when taken together, suggest that NO modulates the expression of caveolin-1 in the brain and that the loss of caveolin-1 is associated with NO production in the ischemic brain. © 2006 International Society for Neurochemistry.
Persistent Identifierhttp://hdl.handle.net/10722/78367
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShen, Jen_HK
dc.contributor.authorMa, Sen_HK
dc.contributor.authorChan, Pen_HK
dc.contributor.authorLee, Wen_HK
dc.contributor.authorFung, PCWen_HK
dc.contributor.authorCheung, RTFen_HK
dc.contributor.authorTong, Yen_HK
dc.contributor.authorLiu, KJen_HK
dc.date.accessioned2010-09-06T07:42:05Z-
dc.date.available2010-09-06T07:42:05Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Neurochemistry, 2006, v. 96 n. 4, p. 1078-1089en_HK
dc.identifier.issn0022-3042en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78367-
dc.description.abstractAs a signalling molecule of the integral membrane protein family, caveolin participates in cellular signal transduction via interaction with other signalling molecules. The nature of interaction between nitric oxide (NO) and caveolin in the brain, however, remains largely unknown. In this study we investigated the role(s) of NO in regulating caveolin-1 expression in rat ischemic brains with middle cerebral artery occlusion (MCAO). Exposure to 1 h ischemia induced the increases in neuronal nitric oxide synthase (nNOS) and NO concentration with concurrent down-regulation of caveolin-1 expression in the ischemic core of rat brains. Subsequent 24 h or more reperfusion time led to an increase in inducible NOS (iNOS) expression and NO production, as well as a decline of caveolin-1 protein at the core and penumbra of the ischemic brain. Afterwards, NOS inhibitors and an NO donor were utilized to clarify the link between NO production and caveolin-1 expression in the rats with 1 h ischemia plus 24 h reperfusion. NG-nitro-l-arginine methyl ester (L-NAME, a non-selective NOS inhibitor), N6-(1-iminoethyl)-lysine (NIL, an iNOS inhibitor), and 7-nitroindazole (7-NI, a nNOS inhibitor) prevented the loss of caveolin-1 in the core and penumbra of the ischemic brain, whereas l-N 5-(1-iminoethyl)-ornithine (L-NIO, an endothelial NOS inhibitor) showed less effect than the other NOS inhibitors. S-Nitroso-N- acetylpenicillamine (SNAP, a NO donor) down-regulated the expression of caveolin-1 protein in normal and ischemic brains. These results, when taken together, suggest that NO modulates the expression of caveolin-1 in the brain and that the loss of caveolin-1 is associated with NO production in the ischemic brain. © 2006 International Society for Neurochemistry.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd.en_HK
dc.relation.ispartofJournal of Neurochemistryen_HK
dc.rightsJournal of Neurochemistry. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectCaveolin-1en_HK
dc.subjectIschemic strokeen_HK
dc.subjectNitric oxideen_HK
dc.subjectNitric oxide synthaseen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBrain Ischemia - physiopathologyen_HK
dc.subject.meshCaveolin 1 - metabolismen_HK
dc.subject.meshEnzyme Inhibitors - pharmacologyen_HK
dc.subject.meshGene Expression Regulation - drug effectsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNG-Nitroarginine Methyl Ester - pharmacologyen_HK
dc.subject.meshNitric Oxide - physiologyen_HK
dc.subject.meshNitric Oxide Donors - pharmacologyen_HK
dc.subject.meshNitric Oxide Synthase - antagonists & inhibitorsen_HK
dc.subject.meshOrnithine - analogs & derivatives - pharmacologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReperfusion Injury - physiopathologyen_HK
dc.titleNitric oxide down-regulates caveolin-1 expression in rat brains during focal cerebral ischemia and reperfusion injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3042&volume=96&issue=4&spage=1078&epage=89&date=2006&atitle=Nitric+oxide+down-regulates+caveolin-1+expression+in+rat+brains+during+focal+cerebral+ischemia+and+reperfusion+injuryen_HK
dc.identifier.emailShen, J: shenjg@hku.hken_HK
dc.identifier.emailMa, S: stefma@hku.hken_HK
dc.identifier.emailCheung, RTF: rtcheung@hku.hken_HK
dc.identifier.emailTong, Y: tongyao@hku.hken_HK
dc.identifier.authorityShen, J=rp00487en_HK
dc.identifier.authorityMa, S=rp00506en_HK
dc.identifier.authorityCheung, RTF=rp00434en_HK
dc.identifier.authorityTong, Y=rp00509en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1471-4159.2005.03589.xen_HK
dc.identifier.pmid16417587-
dc.identifier.scopuseid_2-s2.0-33645107784en_HK
dc.identifier.hkuros119498en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645107784&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume96en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1078en_HK
dc.identifier.epage1089en_HK
dc.identifier.isiWOS:000234975200017-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridShen, J=7404929947en_HK
dc.identifier.scopusauthoridMa, S=16444895800en_HK
dc.identifier.scopusauthoridChan, P=12788250500en_HK
dc.identifier.scopusauthoridLee, W=12788473400en_HK
dc.identifier.scopusauthoridFung, PCW=7101613315en_HK
dc.identifier.scopusauthoridCheung, RTF=7202397498en_HK
dc.identifier.scopusauthoridTong, Y=9045384000en_HK
dc.identifier.scopusauthoridLiu, KJ=7404200456en_HK
dc.identifier.citeulike483489-

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