Tumor necrosis factor-alpha participates in apoptosis in the limbic system after myocardial infarction

Details

Serval ID
serval:BIB_4F183434FB6A
Type
Article: article from journal or magazin.
Collection
Publications
Title
Tumor necrosis factor-alpha participates in apoptosis in the limbic system after myocardial infarction
Journal
Apoptosis
Author(s)
Kaloustian S., Bah T. M., Rondeau I., Mathieu S., Lada-Moldovan L., Ryvlin P., Godbout R., Rousseau G.
ISSN
1573-675X (Electronic)
ISSN-L
1360-8185
Publication state
Published
Issued date
11/2009
Volume
14
Number
11
Pages
1308-16
Language
english
Notes
Kaloustian, S
Bah, T M
Rondeau, I
Mathieu, S
Lada-Moldovan, L
Ryvlin, P
Godbout, R
Rousseau, G
eng
Research Support, Non-U.S. Gov't
Netherlands
Apoptosis. 2009 Nov;14(11):1308-16. doi: 10.1007/s10495-009-0395-x.
Abstract
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.
Keywords
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
Pubmed
Create date
29/11/2018 12:36
Last modification date
20/08/2019 14:04
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