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 journalArticle

156 Citations (Scopus)

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

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Nerve Growth Factor Receptor
NF-kappa B
PC12 Cells
Nerve Growth Factor
Apoptosis
Signal Transduction
Cell Survival
Cell Death
Transcription Factors
Neurons
Cell Line

Keywords

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

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Inhibition of nuclear factor kappa B (NFκB) activity induces nerve growth factor-resistant apoptosis in PC12 cells. / Taglialatela, Giulio; Robinson, Robert; Perez-Polo, J. Regino.

In: Journal of Neuroscience Research, Vol. 47, No. 2, 15.01.1997, p. 155-162.

Research output: Contribution to journalArticle

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