NDLI: Endogenous tumor necrosis factor protects the adult cardiac myocyte against ischemic-induced apoptosis in a murine model of acute myocardial infarction.

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Endogenous tumor necrosis factor protects the adult cardiac myocyte against ischemic-induced apoptosis in a murine model of acute myocardial infarction.

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Endogenous tumor necrosis factor protects the adult cardiac myocyte against ischemic-induced apoptosis in a murine model of acute myocardial infarction.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Taffet, G. E. Kurrelmeyer, K. M. Baumgarten, G. Sivasubramanian, N. Entman, M. L. Mann, D. L. Michael, L. H. Peschon, J. J.
Description	Author Affiliation: Kurrelmeyer KM ( Winters Center for Heart Failure Research, Cardiology Section, Veterans Affairs Medical Center, Houston, TX 77030, USA.);
Abstract	Previous studies have shown that proinflammatory cytokines, such as tumor necrosis factor (TNF), are expressed after acute hemodynamic overloading and myocardial ischemia/infarction. To define the role of TNF in the setting of ischemia/infarction, we performed a series of acute coronary artery occlusions in mice lacking one or both TNF receptors. Left ventricular infarct size was assessed at 24 h after acute coronary occlusion by triphenyltetrazolium chloride (TTC) staining in wild-type (both TNF receptors present) and mice lacking either the type 1 (TNFR1), type 2 (TNFR2), or both TNF receptors (TNFR1/TNFR2). Left ventricular infarct size as assessed by TTC staining was significantly greater (P < 0.005) in the TNFR1/TNFR2-deficient mice (77.2% +/- 15.3%) when compared with either wild-type mice (46.8% +/- 19.4%) or TNFR1-deficient (47.9% +/- 10.6%) or TNFR2-deficient (41.6% +/- 16.5%) mice. Examination of the extent of necrosis in wild-type and TNFR1/TNFR2-deficient mice by anti-myosin Ab staining demonstrated no significant difference between groups; however, the peak frequency and extent of apoptosis were accelerated in the TNFR1/TNFR2-deficient mice when compared with the wild-type mice. The increase in apoptosis in the TNFR1/TNFR2-deficient mice did not appear to be secondary to a selective up-regulation of the Fas ligand/receptor system in these mice. These data suggest that TNF signaling gives rise to one or more cytoprotective signals that prevent and/or delay the development of cardiac myocyte apoptosis after acute ischemic injury.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	10
Volume Number	97
Language	English
Publisher	National Academy of Sciences
Publisher Date	2000-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, CD Physiology Apoptosis Myocardial Infarction Prevention & Control Myocardial Ischemia Physiopathology Myocardium Pathology Receptors, Tumor Necrosis Factor Tumor Necrosis Factor-alpha Acute Disease Animals Genetics Coronary Vessels Disease Models, Animal Mice Mice, Inbred C57BL Mice, Inbred Strains Mice, Knockout Receptors, Tumor Necrosis Factor, Type I Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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