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Title: c-Abl is involved in high glucose-induced apoptosis in embryonic E12.5 cortical neural progenitor cells from the mouse brain
Authors: Jia, D.-Y.
Du, Z.-H.
Liu, S.-M.
Liu, H.-J.
Wang, F.-W.
Ling, E.-A. 
Liu, K.
Hao, A.-J.
Keywords: Apoptosis
High glucose
Neural progenitor cells
Neural tube defects
Reactive oxygen species
Issue Date: Aug-2008
Citation: Jia, D.-Y., Du, Z.-H., Liu, S.-M., Liu, H.-J., Wang, F.-W., Ling, E.-A., Liu, K., Hao, A.-J. (2008-08). c-Abl is involved in high glucose-induced apoptosis in embryonic E12.5 cortical neural progenitor cells from the mouse brain. Journal of Neurochemistry 106 (4) : 1720-1730. ScholarBank@NUS Repository.
Abstract: Hyperglycemia causes direct apoptosis of neural progenitor cells (NPCs) in diabetic-induced neural tube defects in embryos. However, the underlying mechanisms are poorly understood. The present study is aimed to investigate the specific cellular proteins that may be involved in NPCs apoptosis as well as mechanisms by which the proteins regulate the oxidative stress-induced NPCs apoptosis. Our present results have shown that the expression of c-Abl was up-regulated in NPCs exposed to high glucose in vitro. The increased c-Abl was localized mainly in the nucleus. High glucose also induced an increase in nuclear p53 protein levels and the p53-c-Abl complex in NPCs. Administration of reactive oxygen species scavengers decreased the protein level of c-Abl, p53 and NPCs apoptosis. Inhibition of c-Abl reduced NPCs apoptosis and the nuclear protein level of p53 in response to high glucose. These results demonstrate that c-Abl is involved in the reactive oxygen species-activated apoptotic pathways in NPCs apoptosis. Inhibition of c-Abl may protect NPCs against insults induced by high glucose via the modulation of NPCs apoptotic machinery. © 2008 The Authors.
Source Title: Journal of Neurochemistry
ISSN: 00223042
DOI: 10.1111/j.1471-4159.2008.05533.x
Appears in Collections:Staff Publications

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