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Neurology Asia, Volume 18, Issue 4, 2013, pp. 400-407

Myelotomy suppresses autophagic marker LC3-II expression and elevates mTORC1 expression and improves neurological function recovery in rats with spinal cord injury

Yang D. 1, Li J. 1, Hu A. 1, Yang M. 1, Du L. 1, Gao F. 1, Wu Y. 1, He J. 1, Feng Y. 1, Chu H. 1, Gu R. 2, Zhang X. 3, Sun W. 3
Abstract : Although previous studies have shown functional efficacy of myelotomy for the treatment of spinal cord injury (SCI), the underlying mechanism remained unknown. This study aimed to determine the relationship between myelotomy-mediated neuroprotection and autophagy following SCI by evaluating the expression of microtubule-associated protein light chain 3 (LC3-II) and mammalian target of rapamycin complex 1 (mTORC1). Ninety-nine adult female rats were randomly assigned to either sham-operated group (SG), model group (MG), or 24 h-myelotomy group (MTG). SCI at T10 was induced with a New York University impactor, and myelotomy was performed 24 h after SCI. Functional recovery was evaluated via the open-field test. The protein expression of LC3-II was analyzed by Western blot, and the mRNA expression of LC3-II and mTORC1 were detected by real-time quantitative reverse transcriptase polymerase chain reaction. Rats in the MTG exhibited significantly better performance in the hind limbs compared to those in the MG on day seven and fourteen post-injury. Myelotomy suppressed the protein and mRNA expression of LC3-II on day three, seven and fourteen post-injury and increased the mRNA expression of mTORC1 in the MTG on day three and seven post-injury. The LC3-II protein expression was significantly and negatively correlated with BBB scores at day seven and fourteen post-injury. These results showed that myelotomy-induced neuroprotection in a rat model of SCI was likely mediated by inhibition of autophagy by activation of the mTORC1 signaling pathway.
Keywords :
Subject Area : Clinical Neurology Neurology

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