File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Ischemic postconditioning influences electron transport chain protein turnover in Langendorff-perfused rat hearts

TitleIschemic postconditioning influences electron transport chain protein turnover in Langendorff-perfused rat hearts
Authors
KeywordsComparative proteomics
Electron transport chain
Energy homeostasis
Ischemia-reperfusion (I/R) injury
Mitochondrial ATP-sensitive potassium channel (mitoKATP)
Postconditioning
Issue Date2016
PublisherPeerJ, Ltd. The Journal's web site is located at https://peerj.com/
Citation
PeerJ, 2016, v. 4, article no. e1706 How to Cite?
AbstractIschemia postconditioning (IPo) is a promising strategy in reducing myocardial ischemia reperfusion (I/R) injury (MIRI), but its specific molecular mechanism is incompletely understood. Langendorff-perfused isolated rat hearts were subjected to global I/R and received IPo in the absence or presence of the mitochondrial ATP-sensitive potassium channel (mitoKATP) blocker 5-hydroxydecanoate (5-HD). Myocardial mitochondria were extracted and mitochondrial comparative proteomics was analyzed. IPo significantly reduces post-ischemic myocardial infarction and improved cardiac function in I/R rat hearts, while 5-HD basically cancelled IPo’s myocardial protective effect. Joint application of two-dimensional polyacrylamide gel electrophoresis (2DE) and MALDI-TOF MS identified eight differentially expressed proteins between groups. Expression of cardiac succinate dehydrogenase (ubiquinone) flavoprotein subunit (SDHA) increased more than two-fold after I/R, while IPo led to overexpression of dihydrolipoyl dehydrogenase (DLD), NADH dehydrogenase (ubiquinone) flavoprotein 1 and isoform CRA_b (NDUFV1). When the mitoKATP was blocked, MICOS complex subunit Mic60 (IMMT) and Stress-70 protein (Grp75) were over expressed, while DLDH, ATPase subunit A (ATPA) and rCG44606 were decreased. Seven of the differential proteins belong to electron transport chain (ETC) or metabolism regulating proteins, and five of them were induced by closing mitoKATP in I/R hearts. We thus conclude that IPo’s myocardial protective effect relies on energy homeostasis regulation. DLD, SDHA, NDUFV1, Grp75, ATPA and rCG44606 may contribute to IPo’s cardial protective effect.
Persistent Identifierhttp://hdl.handle.net/10722/231627
ISSN
2023 Impact Factor: 2.3
2023 SCImago Journal Rankings: 0.623
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCao, S-
dc.contributor.authorLiu, Y-
dc.contributor.authorWang, H-
dc.contributor.authorMao, X-
dc.contributor.authorChen, J-
dc.contributor.authorLiu, J-
dc.contributor.authorXia, Z-
dc.contributor.authorZhang, L-
dc.contributor.authorLiu, X-
dc.contributor.authorYu, T-
dc.date.accessioned2016-09-20T05:24:27Z-
dc.date.available2016-09-20T05:24:27Z-
dc.date.issued2016-
dc.identifier.citationPeerJ, 2016, v. 4, article no. e1706-
dc.identifier.issn2167-8359-
dc.identifier.urihttp://hdl.handle.net/10722/231627-
dc.description.abstractIschemia postconditioning (IPo) is a promising strategy in reducing myocardial ischemia reperfusion (I/R) injury (MIRI), but its specific molecular mechanism is incompletely understood. Langendorff-perfused isolated rat hearts were subjected to global I/R and received IPo in the absence or presence of the mitochondrial ATP-sensitive potassium channel (mitoKATP) blocker 5-hydroxydecanoate (5-HD). Myocardial mitochondria were extracted and mitochondrial comparative proteomics was analyzed. IPo significantly reduces post-ischemic myocardial infarction and improved cardiac function in I/R rat hearts, while 5-HD basically cancelled IPo’s myocardial protective effect. Joint application of two-dimensional polyacrylamide gel electrophoresis (2DE) and MALDI-TOF MS identified eight differentially expressed proteins between groups. Expression of cardiac succinate dehydrogenase (ubiquinone) flavoprotein subunit (SDHA) increased more than two-fold after I/R, while IPo led to overexpression of dihydrolipoyl dehydrogenase (DLD), NADH dehydrogenase (ubiquinone) flavoprotein 1 and isoform CRA_b (NDUFV1). When the mitoKATP was blocked, MICOS complex subunit Mic60 (IMMT) and Stress-70 protein (Grp75) were over expressed, while DLDH, ATPase subunit A (ATPA) and rCG44606 were decreased. Seven of the differential proteins belong to electron transport chain (ETC) or metabolism regulating proteins, and five of them were induced by closing mitoKATP in I/R hearts. We thus conclude that IPo’s myocardial protective effect relies on energy homeostasis regulation. DLD, SDHA, NDUFV1, Grp75, ATPA and rCG44606 may contribute to IPo’s cardial protective effect.-
dc.languageeng-
dc.publisherPeerJ, Ltd. The Journal's web site is located at https://peerj.com/-
dc.relation.ispartofPeerJ-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectComparative proteomics-
dc.subjectElectron transport chain-
dc.subjectEnergy homeostasis-
dc.subjectIschemia-reperfusion (I/R) injury-
dc.subjectMitochondrial ATP-sensitive potassium channel (mitoKATP)-
dc.subjectPostconditioning-
dc.titleIschemic postconditioning influences electron transport chain protein turnover in Langendorff-perfused rat hearts-
dc.typeArticle-
dc.identifier.emailXia, Z: zyxia@hkucc.hku.hk-
dc.identifier.authorityXia, Z=rp00532-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.7717/peerj.1706-
dc.identifier.pmid26925330-
dc.identifier.pmcidPMC4768691-
dc.identifier.scopuseid_2-s2.0-84963984711-
dc.identifier.hkuros267269-
dc.identifier.volume4-
dc.identifier.spagearticle no. e1706-
dc.identifier.epagearticle no. e1706-
dc.identifier.isiWOS:000370949200005-
dc.publisher.placeUnited States-
dc.identifier.issnl2167-8359-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats