Rat superior cervical ganglion neurons require the presence of nerve growth factor (NGF) to develop and survive in culture. If NGF is removed from the culture medium, then the neurons die of programmed cell death. We investigated the potential role of Ca2+ and reactive oxygen species in this process. We found that overexpression of human wild-type copper/zinc- superoxide dismutase in cultured superior cervical ganglion neurons, using an adenovirus-based vector, substantially protected the cells from the effects of NGF withdrawal, although overexpression of the Ca2+-binding protein calbindin D(28k) or the enzyme β-galactosidase did not. We also observed that treatment of the cells with the cytokine transforming growth factor- β1, which has been shown to protect neurons against oxidative injury, delayed cell death produced by NGF withdrawal. These data suggest a role for reactive oxygen species in triggering programmed cell death of rat sympathetic neurons upon growth factor withdrawal.
|Original language||English (US)|
|Number of pages||6|
|State||Published - 1995|
ASJC Scopus subject areas
- Molecular Medicine