Pharmacological preconditioning with tumor necrosis factor-alpha activates signal transducer and activator of transcription-3 at reperfusion without involving classic prosurvival kinases (Akt and extracellular signal-regulated kinase)

We previously reported that tumor necrosis-factor-alpha (TNF-alpha) can mimic classic ischemic preconditioning (IPC) in a dose- and time-dependent manner. Because TNF-alpha activates the signal transducer and activator of transcription-3 (STAT-3), we hypothesized that TNF-alpha-induced preconditioni...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2005-12, Vol.112 (25), p.3911-3918
Main Authors: Lecour, Sandrine, Suleman, Naushaad, Deuchar, Graeme A, Somers, Sarin, Lacerda, Lydia, Huisamen, Barbara, Opie, Lionel H
Format: Article
Language:English
Subjects:
Animals
Cardiotonic Agents - pharmacology
Cell Survival
In Vitro Techniques
Ischemic Preconditioning, Myocardial - methods
Male
Mitogen-Activated Protein Kinase 3 - metabolism
Myocardial Infarction - prevention & control
Myocardial Reperfusion
Phosphorylation - drug effects
Proto-Oncogene Proteins c-akt - metabolism
Rats
Rats, Wistar
STAT3 Transcription Factor - metabolism
Tumor Necrosis Factor-alpha - pharmacology
Tumor Necrosis Factor-alpha - therapeutic use
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Summary:We previously reported that tumor necrosis-factor-alpha (TNF-alpha) can mimic classic ischemic preconditioning (IPC) in a dose- and time-dependent manner. Because TNF-alpha activates the signal transducer and activator of transcription-3 (STAT-3), we hypothesized that TNF-alpha-induced preconditioning requires phosphorylation of STAT-3 rather than involving the classic prosurvival kinases, Akt and extracellular signal-regulated kinase (Erk) 1/2, during early reperfusion. Isolated, ischemic/reperfused rat hearts were preconditioned by either IPC or low-dose TNF-alpha (0.5 ng/mL). Western blot analysis confirmed that IPC phosphorylated Akt and Erk 1/2 after 5 minutes of reperfusion (Akt increased by 34+/-6% and Erk, by 105+/-28% versus control; P
ISSN:0009-7322
1524-4539
DOI:10.1161/CIRCULATIONAHA.105.581058