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Conference Paper: Vascular smooth muscle cell apoptosis induced by "supercooling" and rewarming

TitleVascular smooth muscle cell apoptosis induced by "supercooling" and rewarming
Authors
Issue Date2006
PublisherElsevier Inc.. The Journal's web site is located at http://www.jvir.org/
Citation
The 30th Annual Meeting of the Southern Association for Vascular Surgery, Phoenix, AZ, 18-21 January 2006. In Journal of Vascular and Interventional Radiology, 2006, v. 17 n. 12, p. 1971-1977 How to Cite?
AbstractPURPOSE: The underlying mechanisms for the reduction in restenosis caused by cryoplasty for peripheral atherosclerotic lesions are not well understood. Because vascular smooth muscle cells (SMCs) are known to play a critical role in restenosis and neointimal hyperplasia, the aim of this study was to determine SMC survival under conditions of "supercooling" and/or rewarming. MATERIALS AND METHODS: Bovine aortic SMCs were supercooled to -10°C for 0, 60, or 120 seconds with a custom-designed conduction cooling stage and then rewarmed to 37°C in an incubator for 0, 12, or 24 hours. A terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay was used to measure the degree of apoptosis. Activation of Akt (ie, protein kinase B), a key signal protein involved in cell survival, was assessed by Western blot analysis. RESULTS: An increase in apoptotic SMCs was observed with increasing supercooling and rewarming time. Akt was significantly activated at only the most severe condition (120 seconds of supercooling and 24 hours of rewarming), which showed a 2.03-fold increase compared with the group without rewarming. CONCLUSIONS: The data suggest that SMC apoptosis occurs with supercooling and rewarming. Protective cell survival mechanisms were activated only late in the rewarming phase. This may partially explain the long-term patency observed with cryoplasty of atherosclerotic peripheral lesions. © Copyright 2006 Society of Cardiovascular & Interventional Radiology.
Persistent Identifierhttp://hdl.handle.net/10722/126923
ISSN
2015 Impact Factor: 2.57
2015 SCImago Journal Rankings: 1.210
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYiu, WKen_HK
dc.contributor.authorCheng, SWKen_HK
dc.contributor.authorSumpio, BEen_HK
dc.date.accessioned2010-10-31T12:56:24Z-
dc.date.available2010-10-31T12:56:24Z-
dc.date.issued2006en_HK
dc.identifier.citationThe 30th Annual Meeting of the Southern Association for Vascular Surgery, Phoenix, AZ, 18-21 January 2006. In Journal of Vascular and Interventional Radiology, 2006, v. 17 n. 12, p. 1971-1977en_HK
dc.identifier.issn1051-0443en_HK
dc.identifier.urihttp://hdl.handle.net/10722/126923-
dc.description.abstractPURPOSE: The underlying mechanisms for the reduction in restenosis caused by cryoplasty for peripheral atherosclerotic lesions are not well understood. Because vascular smooth muscle cells (SMCs) are known to play a critical role in restenosis and neointimal hyperplasia, the aim of this study was to determine SMC survival under conditions of "supercooling" and/or rewarming. MATERIALS AND METHODS: Bovine aortic SMCs were supercooled to -10°C for 0, 60, or 120 seconds with a custom-designed conduction cooling stage and then rewarmed to 37°C in an incubator for 0, 12, or 24 hours. A terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay was used to measure the degree of apoptosis. Activation of Akt (ie, protein kinase B), a key signal protein involved in cell survival, was assessed by Western blot analysis. RESULTS: An increase in apoptotic SMCs was observed with increasing supercooling and rewarming time. Akt was significantly activated at only the most severe condition (120 seconds of supercooling and 24 hours of rewarming), which showed a 2.03-fold increase compared with the group without rewarming. CONCLUSIONS: The data suggest that SMC apoptosis occurs with supercooling and rewarming. Protective cell survival mechanisms were activated only late in the rewarming phase. This may partially explain the long-term patency observed with cryoplasty of atherosclerotic peripheral lesions. © Copyright 2006 Society of Cardiovascular & Interventional Radiology.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc.. The Journal's web site is located at http://www.jvir.org/en_HK
dc.relation.ispartofJournal of Vascular and Interventional Radiologyen_HK
dc.rightsThis is a non-final version of an article published in final form in Journal of Vascular and Interventional Radiology, 2006, v. 17 n. 12, p. 1971-1977-
dc.rightsJournal of Vascular and Interventional Radiology. Copyright © Lippincott Williams & Wilkins.-
dc.subject.meshAnalysis of Variance-
dc.subject.meshAorta, Thoracic - cytology-
dc.subject.meshApoptosis-
dc.subject.meshCold Temperature-
dc.subject.meshMuscle, Smooth, Vascular - cytology-
dc.titleVascular smooth muscle cell apoptosis induced by "supercooling" and rewarmingen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1051-0443&volume=17&issue=12&spage=1971&epage=1977&date=2006&atitle=Vascular+smooth+muscle+cells+apoptosis+induced+by+supercooling+and+re-warming-
dc.identifier.emailYiu, WK: waikiyiu@hku.hken_HK
dc.identifier.emailCheng, SWK: wkcheng@hkucc.hku.hken_HK
dc.identifier.authorityYiu, WK=rp00311en_HK
dc.identifier.authorityCheng, SWK=rp00374en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/01.RVI.0000244868.65867.FBen_HK
dc.identifier.pmid17185696-
dc.identifier.scopuseid_2-s2.0-33847653773en_HK
dc.identifier.hkuros176078en_HK
dc.identifier.hkuros125422-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33847653773&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1971en_HK
dc.identifier.epage1977en_HK
dc.identifier.isiWOS:000243281500016-
dc.publisher.placeUnited Statesen_HK
dc.description.otherThe 30th Annual Meeting of the Southern Association for Vascular Surgery, Phoenix, AZ, 18-21 January 2006. In Journal of Vascular and Interventional Radiology, 2006, v. 17 n. 12, p. 1971-1977-
dc.identifier.scopusauthoridYiu, WK=12763171700en_HK
dc.identifier.scopusauthoridCheng, SWK=7404684779en_HK
dc.identifier.scopusauthoridSumpio, BE=7103201423en_HK

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