TY - JOUR
T1 - Bcl-xLexpression after contusion to the rat spinal cord
AU - Qiu, Jingxin
AU - Nesic, Olivera
AU - Ye, Ziming
AU - Rea, Harriet
AU - Westlund, Karin N.
AU - Xu, Guo Ying
AU - McAdoo, David
AU - Hulsebosch, Clarie E.
AU - Perez-Polo, J. Regino
PY - 2001/11/1
Y1 - 2001/11/1
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Bcl-x
KW - Chronic central pain (CCP)
KW - Spinal cord injury (SCI)
KW - Spinothalamic tract (STT)
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U2 - 10.1089/089771501317095304
DO - 10.1089/089771501317095304
M3 - Article
C2 - 11721745
AN - SCOPUS:0034746732
SN - 0897-7151
VL - 18
SP - 1267
EP - 1278
JO - Central Nervous System Trauma
JF - Central Nervous System Trauma
IS - 11
ER -