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Conference Paper: Essential role of adiponectin in ischemic postconditioning cardioprotection and its association with signal transducer and activator of transcription 3

TitleEssential role of adiponectin in ischemic postconditioning cardioprotection and its association with signal transducer and activator of transcription 3
Authors
Issue Date2014
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Experimental Biology (EB), San Diego, California, USA, 26-30 April 2014. In The FASEB Journal, 2014, v. 28 n. Suppl. 1, p. abstract no. 663.7 How to Cite?
AbstractIschemic postconditioning (IPostC) protects the heart against ischemia reperfusion injury (IRI) by activating signal transducer and activator of transcription 3 (STAT3). Adiponectin (APN), a protein with anti-IRI property, activates STAT3 (Cell Metab. 2011, 13: 401-12), but its role in IPostC is unknown. We postulated that APN is essential for IPostC to confer cardioprotection. Wild type (WT) and APN knockout (KO) mice were subjected to 30 min coronary occlusion followed by 120 min reperfusion without or with IPostC achieved by 3 cycles of 10s of ischemia/10s of reperfusion. Cardiac function was assessed by pressure-volume (PV) loop system. At the end of reperfusion, KO mice displayed larger infarct size and higher plasma creatine kinase-MB, but lower end-systolic PV relation (a reliable measure of ventricular function) and dP/dt (all P<0.05, vs. WT). IPostC significantly attenuated all these changes and increased phosphorylations of cardiac STAT3 (at Ser727), Akt (at Ser473) and eNOS in WT but not in KO mice. In cultured H9C2 cells exposed to 60 min hypoxia (H)/120 min reoxygenation (R), gene silencing with APN or STAT3 siRNA all abolished hypoxic postconditioning (HPostC, 3 cycles of 5 min H/5 min R) mediated cell protection. APN supplementation restored HPostC protection in APN siRNA treated but not in STAT3 siRNA treated cells. We conclude that APN is a key protein for IPostC to activate STAT3 to confer protection.
DescriptionConference Theme: Transforming the Future through Science
Poster Session: Pharmacology and Experimental Therapeutics - Cell Injury/Cell Death
Persistent Identifierhttp://hdl.handle.net/10722/204766
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorLi, Hen_US
dc.contributor.authorIrwin, MGen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2014-09-20T00:39:20Z-
dc.date.available2014-09-20T00:39:20Z-
dc.date.issued2014en_US
dc.identifier.citationExperimental Biology (EB), San Diego, California, USA, 26-30 April 2014. In The FASEB Journal, 2014, v. 28 n. Suppl. 1, p. abstract no. 663.7en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/204766-
dc.descriptionConference Theme: Transforming the Future through Science-
dc.descriptionPoster Session: Pharmacology and Experimental Therapeutics - Cell Injury/Cell Death-
dc.description.abstractIschemic postconditioning (IPostC) protects the heart against ischemia reperfusion injury (IRI) by activating signal transducer and activator of transcription 3 (STAT3). Adiponectin (APN), a protein with anti-IRI property, activates STAT3 (Cell Metab. 2011, 13: 401-12), but its role in IPostC is unknown. We postulated that APN is essential for IPostC to confer cardioprotection. Wild type (WT) and APN knockout (KO) mice were subjected to 30 min coronary occlusion followed by 120 min reperfusion without or with IPostC achieved by 3 cycles of 10s of ischemia/10s of reperfusion. Cardiac function was assessed by pressure-volume (PV) loop system. At the end of reperfusion, KO mice displayed larger infarct size and higher plasma creatine kinase-MB, but lower end-systolic PV relation (a reliable measure of ventricular function) and dP/dt (all P<0.05, vs. WT). IPostC significantly attenuated all these changes and increased phosphorylations of cardiac STAT3 (at Ser727), Akt (at Ser473) and eNOS in WT but not in KO mice. In cultured H9C2 cells exposed to 60 min hypoxia (H)/120 min reoxygenation (R), gene silencing with APN or STAT3 siRNA all abolished hypoxic postconditioning (HPostC, 3 cycles of 5 min H/5 min R) mediated cell protection. APN supplementation restored HPostC protection in APN siRNA treated but not in STAT3 siRNA treated cells. We conclude that APN is a key protein for IPostC to activate STAT3 to confer protection.-
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.titleEssential role of adiponectin in ischemic postconditioning cardioprotection and its association with signal transducer and activator of transcription 3en_US
dc.typeConference_Paperen_US
dc.identifier.emailIrwin, MG: mgirwin@hku.hken_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.authorityIrwin, MG=rp00390en_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.identifier.hkuros235615en_US
dc.identifier.volume28en_US
dc.identifier.issueSuppl. 1en_US
dc.publisher.placeUnited States-

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