Inhibition of nuclear factor kappa B (NFκB) activity induces nerve growth factor-resistant apoptosis in PC12 cells

Giulio Taglialatela, Robert Robinson, J. Regino Perez-Polo

    Research output: Contribution to journalArticlepeer-review

    156 Scopus citations

    Abstract

    The mechanism(s) underlying nerve growth factor (NGF)-mediated rescue of neurons from apoptosis is poorly understood, although it is well established that the high-affinity NGF receptor (TrkA) plays a pivotal role in mediating NGF effects. The report that the low-affinity NGF receptor (p75(NGFR)) can induce apoptosis prompted us to analyze the role played by a putative p75(NGFR)-associated signal-transduction element, the transcription factor nuclear factor kappa B (NFκB), in the modulation of apoptosis in PC12 cells. Here, we report that inhibition of NFκB function results in apoptosis of rat PC12 cells, a neuroblast-like cell line model of NGF-responsive neural tissues. Furthermore, NGF did not protect PC12 cells from cell death induced by the inhibition of NFκB. These results indicate that NFκB function is essential to maintain PC12 cell survival and to permit NGF-mediated rescue, consistent with the idea that signaling elements potentially associated with both TrkA- and p75(NGFR) are involved in the regulation of apoptosis.

    Original languageEnglish (US)
    Pages (from-to)155-162
    Number of pages8
    JournalJournal of Neuroscience Research
    Volume47
    Issue number2
    DOIs
    StatePublished - Jan 15 1997

    Keywords

    • aging
    • neuronal death
    • neurotrophin receptors
    • p75(NGFR)
    • signal transduction

    ASJC Scopus subject areas

    • Cellular and Molecular Neuroscience

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