File Download
  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL

Conference Paper: Adiponectin restores diabetic heart sensitivity to ischemic posctconditioning: role of STAT3 activation

TitleAdiponectin restores diabetic heart sensitivity to ischemic posctconditioning: role of STAT3 activation
Authors
KeywordsBiology
Issue Date2013
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2013 Annual Meeting of Experimental Biology (EB 2013), Boston, MA., 28 March-1 April 2013. In The FASEB Journal, 2013, v. 27 meeting abstracts, no. 1169.10 How to Cite?
AbstractDiabetic hearts are prone to ischemia reperfusion (IR) injury and not sensitivity to ischemic postconditioning (IPostC) cardioprotection, and the mechanism is unclear. Adiponectin (APN) confers cardioprotection in non-diabetes by activating STAT3 (pSTAT3), a key protein in mediating IPostC protection. In diabetic heart, APN is decreased, together with reduced pSTAT3. We hypothesized APN may activate STAT3 in diabetic heart and restore its sensitivity to IPostC. Control (C) and Streptozotocin induced diabetic (D) rats were subjected to 30 min coronary artery ligation followed by 2 hours of reperfusion, without or with IPostC achieved by 3 episodes of 10s reperfusion and 10s re-occlusion at the onset of reperfusion. Rat was injected with APN (1x109pfu) 7 days before inducing IR. Cardiac functions were assessed by pressure volume (PV) conductance system. Post-ischemic myocardial infarct size was higher in D relative to C, together with significant reduction of cardiac pSTAT3 and reduction of end systolic PV relation,a reliable measure of ventricular systolic function, in D rats. All these changes in D were reverted by IPostC in the presence but not in the absence of APN (P<0.05 vs. D+APN+IPostC vs. D or D+APN), and abolished by AG490 (which inhibits STAT3 activation). It is concluded that APN restores diabetic heart sensitivity to IPostC by activating STAT3.
Persistent Identifierhttp://hdl.handle.net/10722/190055
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorLi, Hen_US
dc.contributor.authorWang, Ten_US
dc.contributor.authorLei, Sen_US
dc.contributor.authorNg, KFen_US
dc.contributor.authorIrwin, Men_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2013-09-17T15:06:16Z-
dc.date.available2013-09-17T15:06:16Z-
dc.date.issued2013en_US
dc.identifier.citationThe 2013 Annual Meeting of Experimental Biology (EB 2013), Boston, MA., 28 March-1 April 2013. In The FASEB Journal, 2013, v. 27 meeting abstracts, no. 1169.10en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/190055-
dc.description.abstractDiabetic hearts are prone to ischemia reperfusion (IR) injury and not sensitivity to ischemic postconditioning (IPostC) cardioprotection, and the mechanism is unclear. Adiponectin (APN) confers cardioprotection in non-diabetes by activating STAT3 (pSTAT3), a key protein in mediating IPostC protection. In diabetic heart, APN is decreased, together with reduced pSTAT3. We hypothesized APN may activate STAT3 in diabetic heart and restore its sensitivity to IPostC. Control (C) and Streptozotocin induced diabetic (D) rats were subjected to 30 min coronary artery ligation followed by 2 hours of reperfusion, without or with IPostC achieved by 3 episodes of 10s reperfusion and 10s re-occlusion at the onset of reperfusion. Rat was injected with APN (1x109pfu) 7 days before inducing IR. Cardiac functions were assessed by pressure volume (PV) conductance system. Post-ischemic myocardial infarct size was higher in D relative to C, together with significant reduction of cardiac pSTAT3 and reduction of end systolic PV relation,a reliable measure of ventricular systolic function, in D rats. All these changes in D were reverted by IPostC in the presence but not in the absence of APN (P<0.05 vs. D+APN+IPostC vs. D or D+APN), and abolished by AG490 (which inhibits STAT3 activation). It is concluded that APN restores diabetic heart sensitivity to IPostC by activating STAT3.-
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.titleAdiponectin restores diabetic heart sensitivity to ischemic posctconditioning: role of STAT3 activationen_US
dc.typeConference_Paperen_US
dc.identifier.emailWang, T: wangtt6@hku.hken_US
dc.identifier.emailLei, S: shqlei@hku.hken_US
dc.identifier.emailNg, KF: jkfng@hku.hken_US
dc.identifier.emailIrwin, M: mgirwin@hku.hken_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hken_US
dc.identifier.authorityNg, KF=rp00544en_US
dc.identifier.authorityIrwin, M=rp00390en_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros221911en_US
dc.identifier.volume27en_US
dc.identifier.issuemeeting abstracts-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats