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Conference Paper: Isoflurane preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury via a vascular endothelial growth factor-dependent mechanism

TitleIsoflurane preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury via a vascular endothelial growth factor-dependent mechanism
Authors
KeywordsBiology
Issue Date2012
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Experimental 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
Persistent Identifierhttp://hdl.handle.net/10722/160564
ISSN
2014 Impact Factor: 5.043
2014 SCImago Journal Rankings: 2.516

 

DC FieldValueLanguage
dc.contributor.authorLiu, Yen_US
dc.contributor.authorProcknow, Jen_US
dc.contributor.authorGe, ZDen_US
dc.contributor.authorBienengraeber, Men_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorWarltier, Den_US
dc.contributor.authorPratt, Pen_US
dc.contributor.authorKersten, Jen_US
dc.date.accessioned2012-08-16T06:14:23Z-
dc.date.available2012-08-16T06:14:23Z-
dc.date.issued2012en_US
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. lb525en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/160564-
dc.descriptionOpen Access Journal-
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.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_US
dc.subjectBiology-
dc.titleIsoflurane preconditioning protects cardiomyocytes against hypoxia/reoxygenation injury via a vascular endothelial growth factor-dependent mechanismen_US
dc.typeConference_Paperen_US
dc.identifier.emailLiu, Y: yanan@hku.hken_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hk-
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros205190en_US
dc.identifier.volume26en_US
dc.identifier.issueMeeting abstracts suppl.-
dc.publisher.placeUnited States-
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-

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