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

✍ Scribed by Giulio Taglialatela; Robert Robinson; J. Regino Perez-Polo

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 118 KB
• Volume: 47
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/(sici)1097-4547(19970115)47:2<155::aid-jnr4>3.0.co;2-e

✦ Synopsis

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 (NFkB), in the modulation of apoptosis in PC12 cells. Here, we report that inhibition of NFkB 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 NFkB. These results indicate that NFkB function is essential to maintain PC12 cell survival and to permit NGFmediated rescue, consistent with the idea that signaling elements potentially associated with both TrkAand p75 NGFR are involved in the regulation of apoptosis.