title: Bcl-xL expression after contusion to the rat spinal cord.
abstract: 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-xL, especially among STT cells, consistent with the hypothesis that Bcl-xL regulates the extent of apoptosis after SCI. Apoptosis in the injured spinal cord correlated well with prompt decreases in Bcl-xL protein levels and Bcl-xL/Bax protein ratios at the contusion site. We interpret these results as evidence that regulation of Bcl-xL may play a role in neural sparing after spinal injury and pain-signaling function.
authors.affiliation: Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, USA.
authors.forename: J
authors.initials: J
authors.lastname: Qiu
authors.forename: O
authors.initials: O
authors.lastname: Nesic
authors.forename: Z
authors.initials: Z
authors.lastname: Ye
authors.forename: H
authors.initials: H
authors.lastname: Rea
authors.forename: K N
authors.initials: KN
authors.lastname: Westlund
authors.forename: G Y
authors.initials: GY
authors.lastname: Xu
authors.forename: D
authors.initials: D
authors.lastname: McAdoo
authors.forename: C E
authors.initials: CE
authors.lastname: Hulsebosch
authors.forename: J R
authors.initials: JR
authors.lastname: Perez-Polo
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D015153:Blotting, Western; D003288:Contusions / Q000150:complications / Q000235:genetics* / Q000473:pathology; D004247:DNA / Q000096:biosynthesis / Q000235:genetics; D053938:DNA Fragmentation / Q000502:physiology; D019085:Fluorescent Antibody Technique, Direct; D006657:Histones / Q000378:metabolism; D008124:Locomotion / Q000502:physiology; D008297:Male; D018613:Microscopy, Confocal; D010146:Pain / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D011518:Proto-Oncogene Proteins / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis / Q000235:genetics*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000473:pathology; D013119:Spinal Cord Injuries / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D013133:Spinothalamic Tracts / Q000473:pathology; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein
chemical_list: C494828:Bax protein, rat; C494813:Bcl2l1 protein, rat; D006657:Histones; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein; D004247:DNA