The effects of BclXL and Bax over-expression on stretch-injury induced neural cell death.

Bryan Pfister, George Oyler, Michael Betenbaugh, Gang Bao

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

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, 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 languageEnglish (US)
Pages (from-to)233-243
Number of pages11
JournalMechanics & chemistry of biosystems : MCB
Volume1
Issue number4
StatePublished - Jan 1 2004
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Chemistry (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology (miscellaneous)

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