Document Detail


Ventricular myocyte caspases are directly responsible for endotoxin-induced cardiac dysfunction.
MedLine Citation:
PMID:  15897345     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Although most of the deleterious effects of sepsis-induced apoptosis have been attributed to increased lymphocyte cell death, caspase activation may directly alter cell function of different organ systems. We postulated that left ventricular (LV) cardiomyocyte caspase activation is directly involved in sepsis-induced heart contractile dysfunction. METHODS AND RESULTS: LV cardiomyocytes isolated 4 hours after rat treatment with endotoxin injection (10 mg/kg) displayed major reductions in contractile reserve and myofilament response to Ca2+. Concomitantly, endotoxin also induced increases in LV cardiomyocyte caspase-3, -8, and -9-like activities, which were associated with sarcomeric structure destruction and cleavage of components of the cardiac myofilament. Interestingly, zVAD.fmk treatment of septic rat prevented LV cardiomyocyte contractile dysfunction, reductions in myofilament response to calcium, troponin T cleavage, and sarcomere destruction. Serum (10%) of endotoxin-treated rats induced contractile dysfunction, caspase-3-like activity increase, and troponin T cleavage of naive LV cardiomyocytes. The effects of septic serum were prevented in LV cardiomyocytes isolated from zVAD.fmk- or zDEVD.cmk-treated rats or LV cardiomyocytes preincubated with zVAD.fmk or zDEVD.cmk. CONCLUSIONS: The results show an important relationship between endotoxin-induced caspase activation and reduced contractile reserve and sarcomere disarray at the level of single LV cardiomyocytes.
Authors:
Steve Lancel; Olivier Joulin; Raphael Favory; Jean Francois Goossens; Jérome Kluza; Claude Chopin; Pierre Formstecher; Philippe Marchetti; Remi Neviere
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-05-16
Journal Detail:
Title:  Circulation     Volume:  111     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2005 May 
Date Detail:
Created Date:  2005-05-24     Completed Date:  2006-01-12     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2596-604     Citation Subset:  AIM; IM    
Affiliation:
EA 2689, CHRU, and Université de Lille 2, IFR 114 IMPRT, Lille, France.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / pharmacology
Caspases / metabolism*
Endotoxins / adverse effects*
Heart Diseases / etiology*,  pathology
Heart Ventricles / enzymology,  pathology*
Male
Microfilaments / pathology
Myocardial Contraction
Myocytes, Cardiac / enzymology*
Rats
Rats, Sprague-Dawley
Sarcomeres / pathology
Sepsis / complications,  pathology,  physiopathology*
Troponin T / metabolism
Chemical
Reg. No./Substance:
0/Endotoxins; 0/Troponin T; 7440-70-2/Calcium; EC 3.4.22.-/Caspases

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