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Conference Paper: Ischemia postconditioning attenuates myocardial ischemia reperfusion injury by upregulating cardiac adiponectin expression in mice

TitleIschemia postconditioning attenuates myocardial ischemia reperfusion injury by upregulating cardiac adiponectin expression in mice
Authors
Issue Date2013
PublisherOMICS publishing group. The Journal's web site is located at http://www.omicsonline.org/jdmhome.php
Citation
The 4th World Congress on Diabetes & Metabolism, Chicago, IL., 14-16 August 2013. In Journal of Diabetes & Metabolism, 2013, v. 4 n. 6, p. 109 How to Cite?
AbstractIschemic heart disease (IHD) remains the leading cause of mortality and morbidity in diabetic patients. Ischemia postconditioning (IPostC) has been shown to be a effective way in combating myocardial ischemia-reperfusion injury, but the cardioprotective effects of IpostC is compromised or diminished in patients with diabetes, a metabolic disease that was associated with reduced levels of adiponectin (APN). Adiponectin (APN) is a protein that is secreted primarily from adipose tissue, which confers cardioprotection by enhancing myocardial nitric oxide production, a key mediator in IPostCcardioprotection, however, its role in IPostC mediated cardioprotection has not been investigated. The aims of the present study were to determine the role of APN in IPostC mediated cardioprotective effect and investigate the underlying molecular mechanisms. Wild-type (WT) and APN knockout (AKO) mice were subjected to 30 min coronary artery ligation followed by 2 hours of reperfusion, at the absent or present of IPostC achieved by 3 episodes of 10s reperfusion and 10s re-occlusion immediately after ischemia. Myocardial functions were assessed by pressure volume (PV) conductance system. Post-ischemic myocardial infarct size was higher in AKO relative to WT, which was associate with significant reduction of myocardial p-eNOS expression and end systolic PV relation, a reliable measure of ventricular systolic function, in AKO. In contrast, IPostC significantly reduce infarct size and improve end systolic PV relation, together with significant increase expression of myocardial APN, in WT but not in AKO. It is concluded that enhancement of myocardial APN may represent a key mechanism by which IPostC confers cardioprotection.
DescriptionPoster session
Persistent Identifierhttp://hdl.handle.net/10722/190056
ISSN

 

DC FieldValueLanguage
dc.contributor.authorLi, Hen_US
dc.contributor.authorLiu, Zen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorCheung, CWen_US
dc.contributor.authorWong, GTCen_US
dc.contributor.authorIrwin, MGen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2013-09-17T15:06:17Z-
dc.date.available2013-09-17T15:06:17Z-
dc.date.issued2013en_US
dc.identifier.citationThe 4th World Congress on Diabetes & Metabolism, Chicago, IL., 14-16 August 2013. In Journal of Diabetes & Metabolism, 2013, v. 4 n. 6, p. 109en_US
dc.identifier.issn2155-6156-
dc.identifier.urihttp://hdl.handle.net/10722/190056-
dc.descriptionPoster session-
dc.description.abstractIschemic heart disease (IHD) remains the leading cause of mortality and morbidity in diabetic patients. Ischemia postconditioning (IPostC) has been shown to be a effective way in combating myocardial ischemia-reperfusion injury, but the cardioprotective effects of IpostC is compromised or diminished in patients with diabetes, a metabolic disease that was associated with reduced levels of adiponectin (APN). Adiponectin (APN) is a protein that is secreted primarily from adipose tissue, which confers cardioprotection by enhancing myocardial nitric oxide production, a key mediator in IPostCcardioprotection, however, its role in IPostC mediated cardioprotection has not been investigated. The aims of the present study were to determine the role of APN in IPostC mediated cardioprotective effect and investigate the underlying molecular mechanisms. Wild-type (WT) and APN knockout (AKO) mice were subjected to 30 min coronary artery ligation followed by 2 hours of reperfusion, at the absent or present of IPostC achieved by 3 episodes of 10s reperfusion and 10s re-occlusion immediately after ischemia. Myocardial functions were assessed by pressure volume (PV) conductance system. Post-ischemic myocardial infarct size was higher in AKO relative to WT, which was associate with significant reduction of myocardial p-eNOS expression and end systolic PV relation, a reliable measure of ventricular systolic function, in AKO. In contrast, IPostC significantly reduce infarct size and improve end systolic PV relation, together with significant increase expression of myocardial APN, in WT but not in AKO. It is concluded that enhancement of myocardial APN may represent a key mechanism by which IPostC confers cardioprotection.-
dc.languageengen_US
dc.publisherOMICS publishing group. The Journal's web site is located at http://www.omicsonline.org/jdmhome.php-
dc.relation.ispartofJournal of Diabetes & Metabolismen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleIschemia postconditioning attenuates myocardial ischemia reperfusion injury by upregulating cardiac adiponectin expression in miceen_US
dc.typeConference_Paperen_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.emailCheung, CW: cheucw@hku.hken_US
dc.identifier.emailWong, GTC: gordon@hku.hken_US
dc.identifier.emailIrwin, MG: mgirwin@hku.hken_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityCheung, CW=rp00244en_US
dc.identifier.authorityWong, GTC=rp00523en_US
dc.identifier.authorityIrwin, MG=rp00390en_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.4172/2155-6156.S1.023-
dc.identifier.hkuros221933en_US
dc.identifier.volume4en_US
dc.identifier.issue6en_US
dc.identifier.spage109en_US
dc.identifier.epage109en_US
dc.publisher.placeUnited States-

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