Journal
NEUROSCIENCE LETTERS
Volume 499, Issue 3, Pages 164-169Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2011.05.045
Keywords
E2F1; Cerebellar granule neuron; Apoptosis
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Funding
- National Natural Science Foundation of China [30970922]
- Natural Science Foundation of Guangdong Province [10151018201000011]
- Foundation of Bureau of Health of Guangzhou [2009-YB-154, 201102A213039]
- Foundation of Guangzhou Education Bureau [10A223]
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The transcription factor E2F1 is upregulated when cerebellar granular neurons (CGNs) undergo apoptosis under potassium deprivation. In this study, we examined the effects of E2F1 upregulation on the survival and death of CGNs isolated from C57 mice and Sprague-Dawley (SD) rats. Plasmid- and adenovirus-mediated expression of E2F1 dose-dependently induced apoptosis in mouse CGNs but unexpectedly failed to induce apoptosis in rat CGNs. Caspase 3, a marker for neuronal apoptosis, was significantly activated by ectopic E2F1 expression in mouse CGNs but not in rat CGNs. Furthermore, overexpression of E2F1 significantly promoted apoptotic progression in mouse CGNs following potassium deprivation but attenuated apoptosis in rat CGNs, whereas E2F1 lacking DNA binding ability (E2F1-M132) lost its proapoptotic role in mouse CGNs and anti-apoptotic role in rat CGNs. Together, our results demonstrated that upregulation of E2F1 by potassium deprivation promotes apoptosis in C57 mouse CGNs but antagonizes apoptosis in SD rat CGNs, suggesting opposing roles for E2F1 in regulating CGN fate. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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