Induction of manganese superoxide dismutase in acute spinal cord injury

被引:6
作者
Earnhardt, JN
Streit, WJ
Anderson, DK
O'Steen, WA
Nick, HS
机构
[1] Univ Florida, Dept Neurosci, Coll Med, Gainesville, FL 32610 USA
[2] Univ Florida, Evelyn F & William L McKnight Brain Inst, Gainesville, FL 32610 USA
[3] Malcom Randall Vet Affairs Med Ctr, Gainesville, FL USA
关键词
interleukin-1; beta; MnSOD; motoneuron; spinal cord injury;
D O I
10.1089/089771502760341974
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Free radical-mediated mechanisms of cellular damage have been implicated in the early stages of spinal cord injury (SCI). Manganese superoxide dismutase (MnSOD) is a potent scavenger of superoxide radicals and likely serves an important cytoprotective role in preventing cellular damage after SCI. We have evaluated the expression of MnSOD to address its role during the early events of SCI using a well-established rat contusion model. Northern analysis showed a rapid induction of MnSOD mRNA between 2 and 6 h post injury. Observed time-dependent increases in MnSOD message was maximal 6 h post injury over that of MnSOD mRNA levels induced by laminectomy alone. Immunoblot and immunohistochemical analysis demonstrated increased expression of MnSOD protein 24 h after SCI with localization primarily within neurons. Interestingly, laminectomy alone also caused an induction of MnSOD gene and protein expression. To evaluate one potential mechanism of MnSOD induction, we microinjected the naive spinal cord with IL-1beta, which caused a similar fold induction of MnSOD mRNA levels by 6 h as observed with SCI, thus implicating it as a potential inducer of MnSOD during SCI. In summary, these results demonstrate that this potent cytoprotective antioxidant enzyme is rapidly and significantly induced as a consequence of SCI.
引用
收藏
页码:1065 / 1079
页数:15
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