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Article: Direct comparison of endothelial cell and smooth muscle cell response to supercooling and rewarming

TitleDirect comparison of endothelial cell and smooth muscle cell response to supercooling and rewarming
Authors
Issue Date2007
PublisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/jvs
Citation
Journal Of Vascular Surgery, 2007, v. 46 n. 3, p. 557-564.e2 How to Cite?
AbstractBackground: Cryoplasty combines mechanical dilatation with the delivery of hypothermia to atherosclerotic plaques. The response of vascular smooth muscle cells (SMCs) and endothelial cells (ECs) to supercooling and subsequent rewarming is still not clear. This study investigated the differential effects of vascular cell survival and proliferation in an in vitro model simulating cryoplasty. Methods: Bovine aortic ECs and SMCs were cultured separately with medium supplemented with 10% fetal bovine serum. The samples were supercooled to -10°C for 0, 60, or 120 seconds on a cooling stage and then rewarmed in an incubator at 37°C for 0, 6, 12, or 24 hours. Terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling (TUNEL) and 5′-bromo-2′-deoxyuridine incorporation were used to measure the degree of apoptosis and proliferation respectively. Activation of protein kinase B (AKT), P70 S6 kinase, and P44/42 mitogen-activated protein kinase (MAPK) were assessed by Western blot and quantified using densitometry. Results are given as mean ± standard error of mean and analyzed by analysis of variance. Results: SMC and EC apoptosis were significantly increased with increasing supercooling and rewarming time, with a higher rate in SMCs. SMC apoptosis was maximal at 60 seconds cooling, followed by 24 hours rewarming (17.05% ± 0.44%), whereas maximal EC apoptosis was after 120 seconds cooling, followed by 24 hours rewarming (4.21% ± 0.22%, P < .05). Higher AKT activation was observed in ECs, with a maximum obtained of 3.34-fold at 120 seconds cooling with 24 hours rewarming (P < .05); only modest activation was found in SMCs. ECs had a decreased proliferation with cooling and rewarming time, and although SMCs maintained their low proliferative rate, ECs still had a higher overall proliferation rate that was statistically significant at 60 and 120 seconds cooling without rewarming compared with noncooling and nonrewarming (P < .05). Both p70S6 kinase and p44/42 MAPK activities decreased in SMCs, with significant drop at 60 seconds cooling, followed by 12 hours rewarming (P < .05). However, ECs showed a significant rise of P70 S6 kinase activity at 60 seconds cooling with 12 hours rewarming by 1.62-fold and P44/42 MAPK at 120 seconds cooling with 24 hours rewarming by 1.74-fold (P < .05). Conclusion: The higher apoptosis and lower proliferation of SMCs compared with ECs demonstrate the different effects of supercooling and rewarming on different vascular cell types. This information may be important in helping to understand the mechanism by which cryoplasty of atherosclerotic lesions may result in less restenosis. © 2007 The Society for Vascular Surgery.
Persistent Identifierhttp://hdl.handle.net/10722/172947
ISSN
2015 Impact Factor: 3.454
2015 SCImago Journal Rankings: 2.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYiu, WKen_US
dc.contributor.authorCheng, SWKen_US
dc.contributor.authorSumpio, BEen_US
dc.date.accessioned2012-10-30T06:25:57Z-
dc.date.available2012-10-30T06:25:57Z-
dc.date.issued2007en_US
dc.identifier.citationJournal Of Vascular Surgery, 2007, v. 46 n. 3, p. 557-564.e2en_US
dc.identifier.issn0741-5214en_US
dc.identifier.urihttp://hdl.handle.net/10722/172947-
dc.description.abstractBackground: Cryoplasty combines mechanical dilatation with the delivery of hypothermia to atherosclerotic plaques. The response of vascular smooth muscle cells (SMCs) and endothelial cells (ECs) to supercooling and subsequent rewarming is still not clear. This study investigated the differential effects of vascular cell survival and proliferation in an in vitro model simulating cryoplasty. Methods: Bovine aortic ECs and SMCs were cultured separately with medium supplemented with 10% fetal bovine serum. The samples were supercooled to -10°C for 0, 60, or 120 seconds on a cooling stage and then rewarmed in an incubator at 37°C for 0, 6, 12, or 24 hours. Terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling (TUNEL) and 5′-bromo-2′-deoxyuridine incorporation were used to measure the degree of apoptosis and proliferation respectively. Activation of protein kinase B (AKT), P70 S6 kinase, and P44/42 mitogen-activated protein kinase (MAPK) were assessed by Western blot and quantified using densitometry. Results are given as mean ± standard error of mean and analyzed by analysis of variance. Results: SMC and EC apoptosis were significantly increased with increasing supercooling and rewarming time, with a higher rate in SMCs. SMC apoptosis was maximal at 60 seconds cooling, followed by 24 hours rewarming (17.05% ± 0.44%), whereas maximal EC apoptosis was after 120 seconds cooling, followed by 24 hours rewarming (4.21% ± 0.22%, P < .05). Higher AKT activation was observed in ECs, with a maximum obtained of 3.34-fold at 120 seconds cooling with 24 hours rewarming (P < .05); only modest activation was found in SMCs. ECs had a decreased proliferation with cooling and rewarming time, and although SMCs maintained their low proliferative rate, ECs still had a higher overall proliferation rate that was statistically significant at 60 and 120 seconds cooling without rewarming compared with noncooling and nonrewarming (P < .05). Both p70S6 kinase and p44/42 MAPK activities decreased in SMCs, with significant drop at 60 seconds cooling, followed by 12 hours rewarming (P < .05). However, ECs showed a significant rise of P70 S6 kinase activity at 60 seconds cooling with 12 hours rewarming by 1.62-fold and P44/42 MAPK at 120 seconds cooling with 24 hours rewarming by 1.74-fold (P < .05). Conclusion: The higher apoptosis and lower proliferation of SMCs compared with ECs demonstrate the different effects of supercooling and rewarming on different vascular cell types. This information may be important in helping to understand the mechanism by which cryoplasty of atherosclerotic lesions may result in less restenosis. © 2007 The Society for Vascular Surgery.en_US
dc.languageengen_US
dc.publisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/jvsen_US
dc.relation.ispartofJournal of Vascular Surgeryen_US
dc.rightsJournal of Vascular Surgery. Copyright © Mosby, Inc.-
dc.subject.meshAnimalsen_US
dc.subject.meshAorta, Thoracic - Cytologyen_US
dc.subject.meshApoptosis - Physiologyen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCattleen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCryopreservationen_US
dc.subject.meshDensitometryen_US
dc.subject.meshEndothelial Cells - Cytology - Enzymologyen_US
dc.subject.meshEnzyme Activation - Physiologyen_US
dc.subject.meshIn Situ Nick-End Labelingen_US
dc.subject.meshMitogen-Activated Protein Kinase 1 - Metabolismen_US
dc.subject.meshMitogen-Activated Protein Kinase 3 - Metabolismen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytology - Enzymologyen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshProto-Oncogene Proteins C-Akt - Metabolismen_US
dc.subject.meshRewarmingen_US
dc.titleDirect comparison of endothelial cell and smooth muscle cell response to supercooling and rewarmingen_US
dc.typeArticleen_US
dc.identifier.emailYiu, Wk: waikiyiu@hku.hken_US
dc.identifier.emailCheng, SWK: wkcheng@hkucc.hku.hken_US
dc.identifier.authorityYiu, Wk=rp00311en_US
dc.identifier.authorityCheng, SWK=rp00374en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.jvs.2007.04.072en_US
dc.identifier.pmid17826245-
dc.identifier.scopuseid_2-s2.0-34548435988en_US
dc.identifier.hkuros138353-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34548435988&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume46en_US
dc.identifier.issue3en_US
dc.identifier.spage557en_US
dc.identifier.epage564.e2en_US
dc.identifier.eissn1097-6809-
dc.identifier.isiWOS:000249315500029-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYiu, Wk=12763171700en_US
dc.identifier.scopusauthoridCheng, SWK=7404684779en_US
dc.identifier.scopusauthoridSumpio, BE=7103201423en_US

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