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

Bryan Pfister1, George Oyler2, Michael Betenbaugh3, Gang Bao4
Department of Neurosurgery, University of Pennsylvania, Philadelphia, PA 19104
Department of Biology, University of Maryland at Baltimore County, Baltimore, MD 21210.
Department of Chemical Engineering, The Johns Hopkins University, Baltimore, MD 21218.
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 BclXL 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 BclXL 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.

Cite This Article

Pfister, B., Oyler, G., Betenbaugh, M., Bao, G. (2004). The Effects of BclXL and Bax Over-expression on Stretch-injury Induced Neural Cell Death. Molecular & Cellular Biomechanics, 1(4), 233–244.



This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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