@Article{mcb.2004.001.233,
AUTHOR = {Bryan  Pfister, George  Oyler, Michael  Betenbaugh, Gang  Bao},
TITLE = {The Effects of BclX<sub><i>L</i></sub> and Bax Over-expression on Stretch-injury Induced Neural Cell Death},
JOURNAL = {Molecular \& Cellular Biomechanics},
VOLUME = {1},
YEAR = {2004},
NUMBER = {4},
PAGES = {233--244},
URL = {http://www.techscience.com/mcb/v1n4/33594},
ISSN = {1556-5300},
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<sub><i>L</i></sub> and Bax over-expression on stretch-induced neural cell death using an <i>in vitro</i> uniaxial stretch model of traumatic axonal injury. Specifically, YFP, YFP-tagged Bax and YFP-tagged BclX<sub><i>L</i></sub> 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<sub><i>L</i></sub> 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.},
DOI = {10.3970/mcb.2004.001.233}
}