The Bcl-2 family of proteins has recently been implicated as a possible player in the complex cascade of neural cell death due to traumatic brain injuries. However, it is unclear if the Bcl-2 pathways are activated in mechanically injured neurons. Here we report the effects of BclX(L) and Bax over-expression on stretch-induced neural cell death using an in vitro uniaxial stretch model of traumatic axonal injury. Specifically, YFP, YFP-tagged Bax and YFP-tagged BclX(L) proteins were expressed in differentiated NG108-15 cells and stretch-injury assays were carried out at different strain and strain rate combinations. As a control, insults known to act within the Bcl-2 pathways were used to study cell viability and to compare with the results of cell death due to mechanical stretching. Surprisingly, under the stretch-injury conditions in this study, BclXL did not provide protection against cell death. Further, translocation of Bax could not be identified after stretch-injury. The implications of these findings to cell death pathways in traumatic brain injury are discussed.
|Original language||English (US)|
|Number of pages||11|
|Journal||Mechanics & chemistry of biosystems : MCB|
|State||Published - Jan 1 2004|
All Science Journal Classification (ASJC) codes
- Chemistry (miscellaneous)
- Biochemistry, Genetics and Molecular Biology (miscellaneous)