Document Detail


Thioredoxin redox signaling in the ischemic heart: an insight with transgenic mice overexpressing Trx1.
MedLine Citation:
PMID:  12788387     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study examined if thioredoxin, the major redox-regulator in the mammalian system, plays any role in the redox signaling of ischemic myocardium. Isolated working rat hearts were made globally ischemic for 30 min followed by 2 h of reperfusion. Another group of hearts was rendered tolerant to ischemia by four cyclic episodes of 5 min ischemia each followed by another 10 min of reperfusion. Reperfusion of ischemic myocardium resulted in the downregulation of thioredoxin 1 (Trx1) expression, which was upregulated in the adapted myocardium. The increased expression of Trx1 was completely blocked with cis-diammine-dichloroplatinum (CDDP), an inhibitor of Trx1. CDDP also abolished cardioprotection afforded by ischemic adaptation as evidenced by a reduction of post-ischemic ventricular recovery, increase in myocardial infarct size and cardiomyocyte apoptosis. The decreased amount of reactive oxygen species in the adapted heart was increased significantly, when Trx1 was blocked with CDDP. The cardioprotective role of Trx1 was further confirmed with transgenic mouse hearts overexpressing Trx1. The Trx1 mouse hearts displayed significantly improved post-ischemic ventricular recovery and reduced myocardial infarct size as compared to the corresponding wild-type mouse hearts. Taken together, the results of this study implicate a crucial role of Trx1 in redox signaling of the ischemic myocardium.
Authors:
Tibor Turoczi; Vincent Wen-Hsing Chang; Richard M Engelman; Nilanjana Maulik; Ye Shih Ho; Dipak K Das
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  35     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-06-05     Completed Date:  2004-03-09     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  695-704     Citation Subset:  IM    
Affiliation:
Cardiovascular Research Center, University of Connecticut, School of Medicine, CT 06030 1110, Farmington, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Blotting, Northern
Blotting, Southern
Female
Humans
In Situ Nick-End Labeling
Ischemic Preconditioning, Myocardial
Male
Membrane Proteins / genetics*
Mice
Mice, Transgenic
Myocardial Ischemia*
Myocardial Reperfusion Injury
Myocardium / metabolism
Oxidation-Reduction*
Oxidative Stress
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species
Signal Transduction
Thioredoxins / genetics*,  metabolism*
Time Factors
Up-Regulation
Grant Support
ID/Acronym/Agency:
HL 22559/HL/NHLBI NIH HHS; HL 33889/HL/NHLBI NIH HHS; HL 56803/HL/NHLBI NIH HHS; HL5642/HL/NHLBI NIH HHS; HL63317/HL/NHLBI NIH HHS; P30 ES06639/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Membrane Proteins; 0/Reactive Oxygen Species; 0/Txndc2 protein, mouse; 52500-60-4/Thioredoxins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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