Overexpression of tau leads to the stimulation of neurite outgrowth, the activation of caspase 3 activity, and accumulation and phosphorylation of tau in neuroblastoma cells on cAMP treatment

Neuroscience Research
Chihiro YoshizakiTakashi Yamauchi

Abstract

To explore changes to the tau molecule in Alzheimer's disease, we studied the effect of tau expression in stably transfected neuroblastoma x glioma hybrid NG108-15 cells (tau cells). Tau cells had a similar shape to, but more neurites than, wild type NG108-15 cells (wild type cells). When treated with cAMP, tau cells began to form neurites within 2h. After that, these neurites became longer and thicker than those of wild type cells. An accumulation and increased phosphorylation of tau were observed after 8 h and caspase 3 activity was increased after 4 h in tau cells, but not in wild type cells, upon treatment with cAMP. Caspase 3 activity was activated after the initiation of morphological change, and before the accumulation of tau in tau cells. Under these conditions, apoptotic cell death was not observed and tau was colocalized with tubulin. However, the accumulated tau molecules did not associate with tubulin and were dislocated around and in the nuclei of tau cells. These observations have implications for the cellular causes of Alzheimer's disease where the accumulation and mislocation of tau occur concomitant with neuronal degeneration.

References

Dec 1, 1986·The Journal of Cell Biology·D G Drubin, M W Kirschner
Jan 13, 1995·The Journal of Biological Chemistry·M Morishima-KawashimaY Ihara
Jun 7, 1994·Proceedings of the National Academy of Sciences of the United States of America·A C AlonsoK Iqbal
Feb 9, 1996·Cell·D G Drubin, W J Nelson
Dec 17, 1997·Biochemical and Biophysical Research Communications·R NuydensH Geerts
Aug 28, 1998·Science·N A Thornberry, Y Lazebnik
Oct 24, 1998·Trends in Neurosciences·M G Spillantini, M Goedert
Jun 29, 2000·Annual Review of Biochemistry·W C EarnshawS H Kaufmann
Sep 1, 2000·Brain Research. Brain Research Reviews·L BuéeP R Hof
Mar 29, 2001·Physiological Reviews·D J Selkoe
Jun 7, 2001·Proceedings of the National Academy of Sciences of the United States of America·A AlonsoK Iqbal
Nov 27, 2001·Brain Research·P Mookherjee, G V Johnson
Aug 23, 2002·The Journal of Biological Chemistry·Shinji SatoAkihiko Takashima
Jun 25, 2003·The Journal of Biological Chemistry·Zhiming SuoBarry W Festoff

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Citations

Aug 2, 2007·Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan·Takashi Yamauchi
Oct 6, 2007·Cell Stress & Chaperones·Ari M Chow, Ian R Brown
Jan 19, 2006·Neurochemistry International·Mariko Tsukane, Takashi Yamauchi
Feb 28, 2015·Journal of Alzheimer's Disease : JAD·Huanliang LiuWei Qian
Sep 23, 2014·BioMed Research International·Tom Van DoorenGerard Griffioen
Feb 1, 2007·Journal of Neuroscience Research·Gerardo MorfiniScott T Brady
Jul 31, 2020·Journal of Biochemistry·Chika OguraShoko Nishihara

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