Over-expression of p73β results in apoptotic death of post-mitotic hNT neurons

• Published in: Journal of the neurological sciences Vol. 240; no. 1; pp. 1 - 6
• Main Authors: Jiang, Yuying, Lo, Warren, Akhmametyeva, Elena M., Chang, Long-Sheng
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 15-01-2006; Elsevier Science
• Subjects: Apoptosis; Bax; Biological and medical sciences; Development. Senescence. Regeneration. Transplantation; Fundamental and applied biological sciences. Psychology; Injuries of the nervous system and the skull. Diseases due to physical agents; Medical sciences; Neurology; p57 Kip2; p73; Post-mitotic hNT neurons; Recombinant adenovirus; Traumas. Diseases due to physical agents; Vertebrates: nervous system and sense organs; Post-mitotic hNT neurons; Bax; p57 Kip2; Recombinant adenovirus; p73; Apoptosis; Virus; Nervous system diseases; Adenoviridae; Neuron; Cell death; p57Kip2
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/j.jns.2005.08.012

The p53-related p73 protein is an important mediator of apoptosis, development and tumorigenesis. Previously, we showed that over-expression of the p73β isoform induced apoptosis in proliferating neuronal cells; however, the study did not address the effect of p73 in post-mitotic neurons. To address this question, we used post-mitotic hNT neurons, which have been used as a model of human central nervous system neurons. We found that over-expression of p73β in hNT neurons resulted in apoptosis and an increase in the expression of p57
Kip2 and Bax, but no increase in p53 expression. These results suggest that apoptosis of post-mitotic neurons induced by p73β may involve these mediators. Understanding the regulation of p73 expression will be important for understanding the development of the nervous system and may have implications for the treatment of neurological diseases.