In order to investigate the role of Bcl-2 in dopaminergic cells, we established a dopaminergic neuronal cell line (MN9D) stably expressing human Bcl-2 (MN9D/Bcl-2) or neomycin (MN9D/Neo). Overexpression of Bcl-2 in MN9D cells attenuated cell death due to treatment of mitochondrial electron transport inhibitors including N-methyl-4-phenylpyridinium, whereas it did not prevent cell death induced by reagents generating reactive oxygen species including 6-hydroxy-dopamine. Moreover, the rate of glucose uptake in MN9D/Bcl-2 was significantly lower than that in MN9D/Neo after MPP+ treatment. Thus, Bcl-2 may counter aberrations in mitochondrial electron transfer processes by altering energy metabolism within the MN9D cells.
Bibliographical noteFunding Information:
We thank Drs Stanley J. Korsmeyer, Dennis W. Choi, Richard Todd and J. Koh for thoughtful discussions and critical reading of parts of this manuscript, Dr E. M. Johnson for many valuable discussions and suggestions, and for the use of equipment, and T. L. Deckwerth for his technical assistance. We also gratefully acknowledge Drs A. Heller, L.Wong and D. Hoffman not only for providing us with the MN9D cell line but also for their many insightful comments in using this system. A portion of this work is published in abstract form. Supported by NIA 44626, MH45530 and NS54982.
All Science Journal Classification (ASJC) codes