File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1097/01.RVI.0000244868.65867.FB
- Scopus: eid_2-s2.0-33847653773
- PMID: 17185696
- WOS: WOS:000243281500016
- Find via
Supplementary
- Citations:
- Appears in Collections:
Conference Paper: Vascular smooth muscle cell apoptosis induced by "supercooling" and rewarming
Title | Vascular smooth muscle cell apoptosis induced by "supercooling" and rewarming |
---|---|
Authors | |
Issue Date | 2006 |
Publisher | Elsevier 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 (SAVS 2006), Phoenix, AZ., 18-21 January 2006. In Journal of Vascular and Interventional Radiology, 2006, v. 17 n. 12, p. 1971-1977 How to Cite? |
Abstract | PURPOSE: 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 Identifier | http://hdl.handle.net/10722/126923 |
ISSN | 2023 Impact Factor: 2.6 2023 SCImago Journal Rankings: 0.767 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yiu, WK | en_HK |
dc.contributor.author | Cheng, SWK | en_HK |
dc.contributor.author | Sumpio, BE | en_HK |
dc.date.accessioned | 2010-10-31T12:56:24Z | - |
dc.date.available | 2010-10-31T12:56:24Z | - |
dc.date.issued | 2006 | en_HK |
dc.identifier.citation | The 30th Annual Meeting of the Southern Association for Vascular Surgery (SAVS 2006), Phoenix, AZ., 18-21 January 2006. In Journal of Vascular and Interventional Radiology, 2006, v. 17 n. 12, p. 1971-1977 | en_HK |
dc.identifier.issn | 1051-0443 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/126923 | - |
dc.description.abstract | PURPOSE: 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.language | eng | en_HK |
dc.publisher | Elsevier Inc.. The Journal's web site is located at http://www.jvir.org/ | en_HK |
dc.relation.ispartof | Journal of Vascular and Interventional Radiology | en_HK |
dc.rights | This 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.rights | Journal of Vascular and Interventional Radiology. Copyright © Lippincott Williams & Wilkins. | - |
dc.subject.mesh | Analysis of Variance | - |
dc.subject.mesh | Aorta, Thoracic - cytology | - |
dc.subject.mesh | Apoptosis | - |
dc.subject.mesh | Cold Temperature | - |
dc.subject.mesh | Muscle, Smooth, Vascular - cytology | - |
dc.title | Vascular smooth muscle cell apoptosis induced by "supercooling" and rewarming | en_HK |
dc.type | Conference_Paper | en_HK |
dc.identifier.openurl | http://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.email | Yiu, WK: waikiyiu@hku.hk | en_HK |
dc.identifier.email | Cheng, SWK: wkcheng@hkucc.hku.hk | en_HK |
dc.identifier.authority | Yiu, WK=rp00311 | en_HK |
dc.identifier.authority | Cheng, SWK=rp00374 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1097/01.RVI.0000244868.65867.FB | en_HK |
dc.identifier.pmid | 17185696 | - |
dc.identifier.scopus | eid_2-s2.0-33847653773 | en_HK |
dc.identifier.hkuros | 176078 | en_HK |
dc.identifier.hkuros | 125422 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-33847653773&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 17 | en_HK |
dc.identifier.issue | 12 | en_HK |
dc.identifier.spage | 1971 | en_HK |
dc.identifier.epage | 1977 | en_HK |
dc.identifier.isi | WOS:000243281500016 | - |
dc.publisher.place | United States | en_HK |
dc.description.other | 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 | - |
dc.identifier.scopusauthorid | Yiu, WK=12763171700 | en_HK |
dc.identifier.scopusauthorid | Cheng, SWK=7404684779 | en_HK |
dc.identifier.scopusauthorid | Sumpio, BE=7103201423 | en_HK |
dc.customcontrol.immutable | sml 170324 amended | - |
dc.identifier.issnl | 1051-0443 | - |