NDLI: zVAD-induced necroptosis in L929 cells depends on autocrine production of TNFα mediated by the PKC–MAPKs

Content Provider	PubMed Central
Author	Wu, Y-t Tan, H-l Huang, Q. Sun, X-j Shen, H-m Zhu, X.
Copyright Year	2011
Abstract	It is intriguing that some pan-caspase inhibitors such as zVAD-fmk (zVAD) are capable of inducing necrotic cell death in a selected group of cells. As earlier reports from our laboratory have ruled out the original notion that zVAD-induced necrosis in mouse fibrosarcoma L929 cells was autophagic cell death, the main objective of this study was thus to determine the underlying mechanism of this form of cell death. In this study, we provided clear evidence that zVAD-induced necroptosis in L929 cells and such cell death is dependent on autocrine production of tumor necrosis factor-α (TNFα) at the transcriptional level. More importantly, we identified that activating protein-1 (AP-1), but not nuclear factor κ-B, is the transcription factor controlling zVAD-induced TNFα transcription. Moreover, zVAD is able to activate AP-1 through activation of two upstream mitogen-activated kinases (MAPKs), c-Jun N-terminal kinase and extracellular signal-regulated kinase. Finally, we found that protein kinase C is the important upstream signaling molecule in mediating zVAD-induced activation of MAPKs and AP-1, and subsequent autocrine production of TNFα and cell death. Data from this study reveal the molecular mechanisms underlying zVAD-induced necroptosis, an important form of programmed necrotic cell death with increasing understanding of its biological significance in health and diseases.
Related Links	http://dx.doi.org/10.1038/cdd.2010.72
Ending Page	37
Page Count	12
Starting Page	26
File Format	PDF
ISSN	13509047
e-ISSN	14765403
Journal	Cell Death and Differentiation
Issue Number	1
Volume Number	18
Language	English
Publisher	Nature Publishing Group
Publisher Date	2011-01-01
Access Restriction	Open
Rights Holder	Nature Publishing Group
Subject Keyword	Cell Biology Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology

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