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Published 15 October 2001. doi:10.1083/jcb.200107058
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© The Rockefeller University Press, 0021-9525/2001/10/217 $5.00
The Journal of Cell Biology, Volume 155, Number 2, October 15, 2001 217-226

Article

Apoptotic death of neurons exhibiting peripherin aggregates is mediated by the proinflammatory cytokine tumor necrosis factor-{alpha}



Janice Robertson1,3, Jean-Martin Beaulieu1, Mohammad M. Doroudchi3, Heather D. Durham3, Jean-Pierre Julien1 and Walter E. Mushynski2

1 Centre for Research in Neurosciences, Research Institute of the McGill University Health Centre
2 Department of Biochemistry, McGill University, Montreal, Quebec H3A 2B4, Canada
3 Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada

Address correspondence to Jean-Pierre Julien, Dept. of Neurology, Montreal General Hospital Research Institute, McGill University, 1650 Cedar Ave., Montreal, Quebec H3G 1A4, Canada. Tel.: (514) 937-6011 Ext. 2361. Fax: (514) 934-8265. E-mail: mdju{at}musica.mcgill.ca

Peripherin, a neuronal intermediate filament protein associated with axonal spheroids in amyotrophic lateral sclerosis (ALS), induces the selective degeneration of motor neurons when overexpressed in transgenic mice. To further clarify the selectivity and mechanism of peripherin-induced neuronal death, we analyzed the effects of peripherin overexpression in primary neuronal cultures. Peripherin overexpression led to the formation of cytoplasmic protein aggregates and caused the death not only of motor neurons, but also of dorsal root ganglion (DRG) neurons that were cultured from dissociated spinal cords of peripherin transgenic embryos. Apoptosis of DRG neurons containing peripherin aggregates was dependent on the proinflammatory central nervous system environment of spinal cultures, rich in activated microglia, and required TNF-{alpha}. This synergistic proapoptotic effect may contribute to neuronal selectivity in ALS.

Key Words: peripherin; apoptosis, ALS; neuronal culture; TNF-{alpha}


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