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Conference Paper: Isoflurane preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury via a vascular endothelial growth factor-dependent mechanism
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TitleIsoflurane preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury via a vascular endothelial growth factor-dependent mechanism
 
AuthorsLiu, Y
Procknow, J
Ge, ZD
Bienengraeber, M
Xia, Z
Warltier, D
Pratt, P
Kersten, J
 
KeywordsBiology
 
Issue Date2012
 
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
 
CitationExperimental Biology Annual Meeting (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 Meeting abstracts suppl., abstract no. lb525 [How to Cite?]
 
AbstractIsoflurane preconditioning (IsoPC) has been demonstrated to exert a cardioprotective effect. We aimed to examine the role of vascular endothelial growth factor (VEGF) during cardiomyocyte protection produced by IsoPC. Human coronary endothelial cells(ECs) were co-cultured with cardiomyocytes isolated from neonatal rats. The co-culture underwent 2 hours of hypoxia followed by 2 hours of reoxygenation in the presence or absence of isoflurane administered 60 mins prior to hypoxia. IsoPC significantly increased the production of nitric oxide from ECs and decreased the levels of lactate dehydrogenase release. The beneficial effect of IsoPC on cardiomyocytes was blocked by VEGF neutralizing antibody applied prior to IsoPC. To examine whether VEGF is a downstream target of hypoxia-induced factor 1α (HIF1α), ECs were infected with lentivirus containing shRNA against HIF1α for 72 hours prior to co-culture. The expression of total VEGF and VEGF receptor 2 proteins was significantly decreased by HIF1α knockdown. IsoPC failed to protect cardiomyocyte against hypoxia/reoxygenation (H/R) injury in HIF1α knockdown ECs. The detrimental effect of HIF1α silencing on IsoPC was restored by administration of recombinant VEGF during the period of co-culturing. These results demonstrate that VEGF plays a critical role in cardiomyocyte protection against H/R injury. During IsoPC, VEGF may be a downstream mediator of HIF1α.
 
DescriptionOpen Access Journal
 
ISSN0892-6638
2012 Impact Factor: 5.704
2012 SCImago Journal Rankings: 2.500
 
DC FieldValue
dc.contributor.authorLiu, Y
 
dc.contributor.authorProcknow, J
 
dc.contributor.authorGe, ZD
 
dc.contributor.authorBienengraeber, M
 
dc.contributor.authorXia, Z
 
dc.contributor.authorWarltier, D
 
dc.contributor.authorPratt, P
 
dc.contributor.authorKersten, J
 
dc.date.accessioned2012-08-16T06:14:23Z
 
dc.date.available2012-08-16T06:14:23Z
 
dc.date.issued2012
 
dc.description.abstractIsoflurane preconditioning (IsoPC) has been demonstrated to exert a cardioprotective effect. We aimed to examine the role of vascular endothelial growth factor (VEGF) during cardiomyocyte protection produced by IsoPC. Human coronary endothelial cells(ECs) were co-cultured with cardiomyocytes isolated from neonatal rats. The co-culture underwent 2 hours of hypoxia followed by 2 hours of reoxygenation in the presence or absence of isoflurane administered 60 mins prior to hypoxia. IsoPC significantly increased the production of nitric oxide from ECs and decreased the levels of lactate dehydrogenase release. The beneficial effect of IsoPC on cardiomyocytes was blocked by VEGF neutralizing antibody applied prior to IsoPC. To examine whether VEGF is a downstream target of hypoxia-induced factor 1α (HIF1α), ECs were infected with lentivirus containing shRNA against HIF1α for 72 hours prior to co-culture. The expression of total VEGF and VEGF receptor 2 proteins was significantly decreased by HIF1α knockdown. IsoPC failed to protect cardiomyocyte against hypoxia/reoxygenation (H/R) injury in HIF1α knockdown ECs. The detrimental effect of HIF1α silencing on IsoPC was restored by administration of recombinant VEGF during the period of co-culturing. These results demonstrate that VEGF plays a critical role in cardiomyocyte protection against H/R injury. During IsoPC, VEGF may be a downstream mediator of HIF1α.
 
dc.description.naturelink_to_OA_fulltext
 
dc.descriptionOpen Access Journal
 
dc.description.otherExperimental Biology Annual Meeting (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 Meeting abstracts suppl., abstract no. lb525
 
dc.identifier.citationExperimental Biology Annual Meeting (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 Meeting abstracts suppl., abstract no. lb525 [How to Cite?]
 
dc.identifier.hkuros205190
 
dc.identifier.issn0892-6638
2012 Impact Factor: 5.704
2012 SCImago Journal Rankings: 2.500
 
dc.identifier.issueMeeting abstracts suppl.
 
dc.identifier.urihttp://hdl.handle.net/10722/160564
 
dc.identifier.volume26
 
dc.languageeng
 
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofThe FASEB Journal
 
dc.subjectBiology
 
dc.titleIsoflurane preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury via a vascular endothelial growth factor-dependent mechanism
 
dc.typeConference_Paper
 
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<description.abstract>Isoflurane preconditioning (IsoPC) has been demonstrated to exert a cardioprotective effect. We aimed to examine the role of vascular endothelial growth factor (VEGF) during cardiomyocyte protection produced by IsoPC. Human coronary endothelial cells(ECs) were co-cultured with cardiomyocytes isolated from neonatal rats. The co-culture underwent 2 hours of hypoxia followed by 2 hours of reoxygenation in the presence or absence of isoflurane administered 60 mins prior to hypoxia. IsoPC significantly increased the production of nitric oxide from ECs and decreased the levels of lactate dehydrogenase release. The beneficial effect of IsoPC on cardiomyocytes was blocked by VEGF neutralizing antibody applied prior to IsoPC. To examine whether VEGF is a downstream target of hypoxia-induced factor 1&#945; (HIF1&#945;), ECs were infected with lentivirus containing shRNA against HIF1&#945; for 72 hours prior to co-culture. The expression of total VEGF and VEGF receptor 2 proteins was significantly decreased by HIF1&#945; knockdown. IsoPC failed to protect cardiomyocyte against hypoxia/reoxygenation (H/R) injury in HIF1&#945; knockdown ECs. The detrimental effect of HIF1&#945; silencing on IsoPC was restored by administration of recombinant VEGF during the period of co-culturing. These results demonstrate that VEGF plays a critical role in cardiomyocyte protection against H/R injury. During IsoPC, VEGF may be a downstream mediator of HIF1&#945;.</description.abstract>
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