Document Detail


Metabolomic analysis of two different models of delayed preconditioning.
MedLine Citation:
PMID:  23127662     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recently we described an ischemic preconditioning induced by repetitive coronary stenosis, which is induced by 6 episodes of non-lethal ischemia over 3 days, and which also resembles the hibernating myocardium phenotype. When compared with traditional second window of ischemic preconditioning using cDNA microarrays, many genes which differed in the repetitive coronary stenosis appeared targeted to metabolism. Accordingly, the goal of this study was to provide a more in depth analysis of changes in metabolism in the different models of delayed preconditioning, i.e., second window and repetitive coronary stenosis. This was accomplished using a metabolomic approach based on liquid chromatography-mass spectrometry (LC-MS) and gas chromatography-mass spectrometry (GC-MS) techniques. Myocardial samples from the ischemic section of porcine hearts subjected to both models of late preconditioning were compared against sham controls. Interestingly, although both models involve delayed preconditioning, their metabolic signatures were radically different; of the total number of metabolites that changed in both models (135 metabolites) only 7 changed in both models, and significantly more, p<0.01, were altered in the repetitive coronary stenosis (40%) than in the second window (8.1%). The most significant changes observed were in energy metabolism, e.g., phosphocreatine was increased 4 fold and creatine kinase activity increased by 27.2%, a pattern opposite from heart failure, suggesting that the repetitive coronary stenosis and potentially hibernating myocardium have enhanced stress resistance capabilities. The improved energy metabolism could also be a key mechanism contributing to the cardioprotection observed in the repetitive coronary stenosis and in hibernating myocardium. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism".
Authors:
Claudio Bravo; Raymond K Kudej; Chujun Yuan; Seonghun Yoon; Hui Ge; Ji Yeon Park; Bin Tian; William C Stanley; Stephen F Vatner; Dorothy E Vatner; Lin Yan
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-11-02
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  55     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-01-28     Completed Date:  2013-07-03     Revised Date:  2014-04-10    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  19-26     Citation Subset:  IM    
Copyright Information:
Copyright © 2012. Published by Elsevier Ltd.
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MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal
Female
Ischemic Preconditioning, Myocardial* / methods
Metabolic Networks and Pathways
Metabolome*
Metabolomics*
Myocardial Ischemia / metabolism
Myocardium / metabolism*
Principal Component Analysis
Swine
Grant Support
ID/Acronym/Agency:
P01 AG027211/AG/NIA NIH HHS; P01 HL069020/HL/NHLBI NIH HHS; P01AG027211/AG/NIA NIH HHS; P01HL069020/HL/NHLBI NIH HHS; R01 HL033107/HL/NHLBI NIH HHS; R01 HL091781/HL/NHLBI NIH HHS; R01 HL093415/HL/NHLBI NIH HHS; R01 HL093481/HL/NHLBI NIH HHS; R01 HL095888/HL/NHLBI NIH HHS; R01 HL102472/HL/NHLBI NIH HHS; R01 HL106511/HL/NHLBI NIH HHS; R01HL033107/HL/NHLBI NIH HHS; R01HL091781/HL/NHLBI NIH HHS; R01HL093415/HL/NHLBI NIH HHS; R01HL093481/HL/NHLBI NIH HHS; R01HL095888/HL/NHLBI NIH HHS; R01HL102472/HL/NHLBI NIH HHS; R01HL106511/HL/NHLBI NIH HHS; R37 HL033107/HL/NHLBI NIH HHS; T32 HL069752/HL/NHLBI NIH HHS; T32HL069752/HL/NHLBI NIH HHS
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