Abstract:
:Bax, a member of the Bcl-2 gene family, is known to promote apoptosis in many cases but to block cell death under certain conditions. To investigate the potential role of Bax in 6-hydroxydopamine (6-OHDA)-induced cell death, we first established and characterized a dopaminergic neuronal cell line (MN9D) stably overexpressing hemagglutinin epitope-tagged Bax (MN9D/HA-Bax) as well as control clones (MN9D/Neo). Treatment of MN9D/Neo cells with 6-OHDA induced typical apoptotic cell death accompanied by shrinkage of the cell, nuclear condensation, and DNA fragmentation as demonstrated by light microscopy and agarose gel analysis. Overexpression of HA-Bax in MN9D cells was shown to attenuate 6-OHDA-induced cell death as determined by the MTT reduction assay and agarose gel analysis for DNA fragmentation. Western blot analysis revealed that cleavage of poly(ADP-ribose)polymerase induced by 6-OHDA was attenuated in MN9D/HA-Bax cells. In contrast, overexpression of a well-known cell death-inhibiting protein such as Bcl-2 or Bcl-XL did not attenuate 6-OHDA-induced cell death. Interestingly, cell death induced by hydrogen peroxide (0.25-2.0 mM) was significantly accelerated, whereas the rate of cell death induced by menadione (10-50 microM) was not affected in MN9D/HA-Bax cells. Thus, our present data suggest that the functionally diverse roles of Bax may be determined by the type of stress applied to the cell.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Oh JH,Choi WS,Kim JE,Seo JW,O'Malley KL,Oh YJdoi
10.1006/exnr.1998.6923subject
Has Abstractpub_date
1998-11-01 00:00:00pages
193-8issue
1eissn
0014-4886issn
1090-2430pii
S0014-4886(98)96923-0journal_volume
154pub_type
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