Document Detail


Tumor necrosis factor-alpha participates in apoptosis in the limbic system after myocardial infarction.
MedLine Citation:
PMID:  19728097     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study was designed to determine the role of tumor necrosis factor-alpha (TNFalpha) in apoptosis observed in the myocardium and limbic system after myocardial ischemia. PEG sTNFRI, a recombinant, human, soluble p55 Type 1 TNF receptor (3 mg/kg) or vehicle (saline) was administered s.c. to male Sprague-Dawley rats on days 5, 3 and 1 before myocardial ischemia. The animals were then subjected, under anesthesia, to left anterior descending coronary artery occlusion for 40 min, followed by 15-min or 72-h reperfusion. Caspase-3 and -8 activities as well as terminal dUTP nick-end labelling-positive cells were examined in the myocardium (subendocardial and subepicardial regions), lateral (LA) and medial amygdala (MA) and hippocampus (CA1, CA3, dentate gyrus (DG)). After 15 min of reperfusion, the subendocardial and CA1 regions presented an increase in caspase-3 activity, whereas caspase-8 activity appeared to be augmented in the DG. PEG sTNFRI inhibited caspase-8 activation in the DG. After 72 h of reperfusion, plasma TNFalpha levels were reduced in the treated groups. The DG, CA1, CA3 and MA showed an increment of caspase-8 activity, which was reversed by PEG sTNFRI, except in the MA. Furthermore, caspase-3 activity was increased in the CA1, DG, LA and MA. These results indicate that TNFalpha contributes to apoptosis via activation of the extrinsic pathway in the limbic system after myocardial infarction, which is not the case in the myocardium.
Authors:
S Kaloustian; T M Bah; I Rondeau; S Mathieu; L Lada-Moldovan; P Ryvlin; R Godbout; G Rousseau
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Apoptosis : an international journal on programmed cell death     Volume:  14     ISSN:  1573-675X     ISO Abbreviation:  Apoptosis     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2010-01-29     Completed Date:  2010-03-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9712129     Medline TA:  Apoptosis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1308-16     Citation Subset:  IM    
Affiliation:
D?partement de pharmacologie, Universit? de Montr?al, Qu?bec, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects,  physiology*
Caspase 3 / metabolism
Caspase 8 / metabolism
Humans
In Situ Nick-End Labeling
Limbic System / pathology*
Male
Myocardial Infarction / pathology*
Myocardium / enzymology
Rats
Rats, Sprague-Dawley
Receptors, Tumor Necrosis Factor / physiology
Tumor Necrosis Factor-alpha / blood,  metabolism*
Chemical
Reg. No./Substance:
0/Receptors, Tumor Necrosis Factor; 0/Tumor Necrosis Factor-alpha; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8

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


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