Novel Shift of Jak/Stat Signalling Characterizes the Protective Effect of Aurintricarboxylic Acid (ATA) from Tumor Necrosis Factor-α Toxicity in Human B Lymphocytes

Previous results demonstrated that the occurrence of death in human peripheral B lymphocytes by TNF-a was paralleled by the activation of the cytoplasmic Jak1 and Tyk2 protein kinases, along with the recruitment of transcription factors Stat3 and Stat5b. In this study we demonstrate that the balance...

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Bibliographic Details
Published in:International journal of immunopathology and pharmacology 2004-01, Vol.17 (1), p.5-14
Main Authors: Marchisio, M., Grimley, P. M., Di Baldassarre, A., Santavenere, E., Miscia, S.
Format: Article
Language:English
Subjects:
Aurintricarboxylic Acid - pharmacology
B-Lymphocytes - cytology
B-Lymphocytes - drug effects
B-Lymphocytes - enzymology
B-Lymphocytes - physiology
Cell Death - drug effects
Cell Death - physiology
Cell Survival - drug effects
Cell Survival - physiology
Cells, Cultured
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Humans
Janus Kinase 1
NF-kappa B - physiology
Protein-Tyrosine Kinases - physiology
Signal Transduction - physiology
STAT3 Transcription Factor
Trans-Activators - genetics
Trans-Activators - metabolism
Tumor Necrosis Factor-alpha - toxicity
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Summary:Previous results demonstrated that the occurrence of death in human peripheral B lymphocytes by TNF-a was paralleled by the activation of the cytoplasmic Jak1 and Tyk2 protein kinases, along with the recruitment of transcription factors Stat3 and Stat5b. In this study we demonstrate that the balance of survival signals in the presence of TNF-α was altered by the addition of a salicylate compound, the endonuclease inhibitor aurintricarboxylic acid (ATA). Apoptosis effected by TNF-α alone was suppressed by ATA and this event was paralleled by phosphorylation and nuclear translocation of Jak2, Stat2, Stat4 and NF-kB, along with inhibition of caspase activation. These results confirm that among the different cellular responses evoked by TNF-α in human B cells, recruitment of Jak/Stat proteins and possible related gene modulation represent contributing factors and address the issue of the development of potential therapeutic strategies aimed at the control of systemic or local effects produced by TNF-α.
ISSN:0394-6320
2058-7384
DOI:10.1177/039463200401700102