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Article: Vascular endothelial growth factor regulation of endothelial nitric oxide synthase phosphorylation is involved in isoflurane cardiac preconditioning

TitleVascular endothelial growth factor regulation of endothelial nitric oxide synthase phosphorylation is involved in isoflurane cardiac preconditioning
Authors
KeywordsVascular endothelial growth factor
Endothelial nitric oxide synthase
Cardiac Preconditioning
Ischaemia/reperfusion
Issue Date2019
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 2019, v. 115 n. 1, p. 168-178 How to Cite?
AbstractAims: Previous studies indicate that nitric oxide derived from endothelial nitric oxide synthase (eNOS) serves as both trigger and mediator in anaesthetic cardiac preconditioning. The mechanisms underlying regulation of eNOS by volatile anaesthetics have not been fully understood. Therefore, this study examined the role of vascular endothelial growth factor (VEGF) in isoflurane cardiac preconditioning. Methods and results: Wistar rats underwent 30 min of coronary artery occlusion followed by 2 h of reperfusion. Isoflurane given prior to ischaemia/reperfusion significantly decreased myocardial infarct size from 60 ± 1% in control to 40 ± 3% (n = 8 rats/group, P < 0.05). The beneficial effects of isoflurane were blocked by neutralizing antibody against VEGF (nVEGF). Coronary arterial endothelial cells (ECs) alone or together with cardiomyocytes (CMs) were subjected to hypoxia/reoxygenation injury. The expression of VEGF and eNOS was analysed by western blot, and nitric oxide was measured by ozone-based chemiluminescence. In co-cultured CMs and ECs, isoflurane administered before hypoxia/reoxygenation attenuated lactate dehydrogenase activity and increased the ratio of phosphorylated eNOS/eNOS and nitric oxide production. The protective effect of isoflurane on CMs was compromised by nVEGF and after VEGF in ECs was inhibited with hypoxia inducible factor-1α short hairpin RNA (shRNA). The negative effect of hypoxia inducible factor-1α shRNA was restored by recombinant VEGF. Conclusion: Isoflurane cardiac preconditioning is associated with VEGF regulation of phosphorylation of eNOS and nitric oxide production.
Persistent Identifierhttp://hdl.handle.net/10722/258541
ISSN
2023 Impact Factor: 10.2
2023 SCImago Journal Rankings: 2.809
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLiu, Y-
dc.contributor.authorPaterson, M-
dc.contributor.authorBaumgardt, SL-
dc.contributor.authorIrwin, MG-
dc.contributor.authorXia, Z-
dc.contributor.authorBosnjak, ZJ-
dc.contributor.authorGe, Z-
dc.date.accessioned2018-08-22T01:40:10Z-
dc.date.available2018-08-22T01:40:10Z-
dc.date.issued2019-
dc.identifier.citationCardiovascular Research, 2019, v. 115 n. 1, p. 168-178-
dc.identifier.issn0008-6363-
dc.identifier.urihttp://hdl.handle.net/10722/258541-
dc.description.abstractAims: Previous studies indicate that nitric oxide derived from endothelial nitric oxide synthase (eNOS) serves as both trigger and mediator in anaesthetic cardiac preconditioning. The mechanisms underlying regulation of eNOS by volatile anaesthetics have not been fully understood. Therefore, this study examined the role of vascular endothelial growth factor (VEGF) in isoflurane cardiac preconditioning. Methods and results: Wistar rats underwent 30 min of coronary artery occlusion followed by 2 h of reperfusion. Isoflurane given prior to ischaemia/reperfusion significantly decreased myocardial infarct size from 60 ± 1% in control to 40 ± 3% (n = 8 rats/group, P < 0.05). The beneficial effects of isoflurane were blocked by neutralizing antibody against VEGF (nVEGF). Coronary arterial endothelial cells (ECs) alone or together with cardiomyocytes (CMs) were subjected to hypoxia/reoxygenation injury. The expression of VEGF and eNOS was analysed by western blot, and nitric oxide was measured by ozone-based chemiluminescence. In co-cultured CMs and ECs, isoflurane administered before hypoxia/reoxygenation attenuated lactate dehydrogenase activity and increased the ratio of phosphorylated eNOS/eNOS and nitric oxide production. The protective effect of isoflurane on CMs was compromised by nVEGF and after VEGF in ECs was inhibited with hypoxia inducible factor-1α short hairpin RNA (shRNA). The negative effect of hypoxia inducible factor-1α shRNA was restored by recombinant VEGF. Conclusion: Isoflurane cardiac preconditioning is associated with VEGF regulation of phosphorylation of eNOS and nitric oxide production.-
dc.languageeng-
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org-
dc.relation.ispartofCardiovascular Research-
dc.subjectVascular endothelial growth factor-
dc.subjectEndothelial nitric oxide synthase-
dc.subjectCardiac Preconditioning-
dc.subjectIschaemia/reperfusion-
dc.titleVascular endothelial growth factor regulation of endothelial nitric oxide synthase phosphorylation is involved in isoflurane cardiac preconditioning-
dc.typeArticle-
dc.identifier.emailIrwin, MG: mgirwin@hku.hk-
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hk-
dc.identifier.authorityIrwin, MG=rp00390-
dc.identifier.authorityXia, Z=rp00532-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/cvr/cvy157-
dc.identifier.pmid29931049-
dc.identifier.pmcidPMC6302266-
dc.identifier.scopuseid_2-s2.0-85058917907-
dc.identifier.hkuros287525-
dc.identifier.hkuros300370-
dc.identifier.volume115-
dc.identifier.issue1-
dc.identifier.spage168-
dc.identifier.epage178-
dc.identifier.isiWOS:000462749000023-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl0008-6363-

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