Open Access

ARTICLE

The Effects of BclX_L and Bax Over-expression on Stretch-injury Induced Neural Cell Death

Bryan Pfister¹, George Oyler², Michael Betenbaugh³, Gang Bao⁴

1 Department of Neurosurgery, University of Pennsylvania, Philadelphia, PA 19104
2 Department of Biology, University of Maryland at Baltimore County, Baltimore, MD 21210.
3 Department of Chemical Engineering, The Johns Hopkins University, Baltimore, MD 21218.
4 Department of Biomedical Engineering, Georgia Instituteof Technology and Emory University, Atlanta, GA 30332, gang.bao@bme.gatech.edu

Molecular & Cellular Biomechanics 2004, 1(4), 233-244. https://doi.org/10.3970/mcb.2004.001.233

Abstract

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, BclX_L 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.

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