Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, United States.
Neurosci Lett. 2009 Nov 20;465(3):226-9. doi: 10.1016/j.neulet.2009.09.013. Epub 2009 Sep 17.
Bone morphogenetic protein 7 (BMP7) has been shown to ameliorate reduced dendritic growth induced by glutamate excitotoxicity in neuronal tissue cultures and/or provide an enhancement of functional recovery in central nervous system (CNS) injury. BMP7 expression is modulated by spinal cord injury (SCI), but the molecular mechanisms involved in neuroprotection have not been clearly defined. Here, we show that BMP7 treatment of rats subjected to mild cervical SCI significantly increased the pro-survival mitogen-activated protein kinase-38 (MAPK-38) pathway and levels of N-methyl-D-aspartate receptor 1 (NMDAR-1) resulting in a significant increase in neuronal sparing in the ventral horn of the spinal cord. Moreover, BMP7 was neuroprotective against glutamate-mediated excitotoxicity in cultured cortical neurons. These studies show that BMP7 administration may be used as a therapeutic strategy to reduce the damaging excitotoxic effects following SCI.
骨形态发生蛋白 7(BMP7)已被证明可以改善神经元组织培养中谷氨酸兴奋性毒性诱导的树突生长减少,并/或增强中枢神经系统(CNS)损伤的功能恢复。BMP7 的表达受脊髓损伤(SCI)调节,但神经保护涉及的分子机制尚未明确界定。在这里,我们表明,BMP7 治疗轻度颈 SCI 大鼠可显著增加促生存丝裂原活化蛋白激酶-38(MAPK-38)途径和 N-甲基-D-天冬氨酸受体 1(NMDAR-1)的水平,从而导致脊髓腹角的神经元保留显著增加。此外,BMP7 对培养的皮质神经元中的谷氨酸介导的兴奋性毒性具有神经保护作用。这些研究表明,BMP7 的给药可作为一种治疗策略,以减少 SCI 后破坏性的兴奋性毒性作用。