Bcl-xLexpression after contusion to the rat spinal cord

Jingxin Qiu, Olivera Nesic, Ziming Ye, Harriet Rea, Karin N. Westlund, Guo Ying Xu, David McAdoo, Clarie E. Hulsebosch, J. Regino Perez-Polo

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    35 Scopus citations


    After contusion-derived spinal cord injury, (SCI) there is localized tissue disruption and energy failure that results in early necrosis and delayed apoptosis, events that contribute to chronic central pain in a majority of patients. We assessed the extent of contusion-induced apoptosis of neurons in a known central pain-signaling pathway, the spinothalamic tract (STT), which may be a contributor to SCI-induced pain. We observed the loss of STT cells and localized increase of DNA fragmentation and cytoplasmic histone-DNA complexes, which suggested potential apoptotic changes among STT neurons after SCI. We also showed SCI-associated changes in the expression of the antiapoptotic protein Bcl-xLespecially among STT cells, consistent with the hypothesis that Bcl-xLregulates the extent of apoptosis after SCI. Apoptosis in the injured spinal cord correlated well with prompt decreases in Bcl-xLprotein levels and Bcl-xL/Bax protein ratios at the contusion site. We interpret these results as evidence that regulation of Bcl-xLmay play a role in neural sparing after spinal injury and pain-signaling function.

    Original languageEnglish (US)
    Pages (from-to)1267-1278
    Number of pages12
    JournalJournal of neurotrauma
    Issue number11
    StatePublished - Nov 1 2001


    • Apoptosis
    • Bcl-x
    • Chronic central pain (CCP)
    • Spinal cord injury (SCI)
    • Spinothalamic tract (STT)

    ASJC Scopus subject areas

    • Clinical Neurology


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