ProNGF induces p75-mediated death of oligodendrocytes following spinal cord injury
ProNGF induces p75-mediated death of oligodendrocytes following spinal cord injury
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DOI：
10.1016/s0896-6273(02)01005-x
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发表时间：
2002-10-24
期刊：
影响因子：
16.2
通讯作者：
Yoon, SO
中科院分区：
文献类型：
--
作者：
Beattie, MS;Harrington, AW;Yoon, SO
神经营养因子受体p75可由神经系统的各种损伤诱导，但其在损伤后的作用尚不清楚。在这里，我们报道p75是脊髓损伤后少突胶质细胞死亡所必需的，其作用主要由proNGF介导。发生凋亡的少突胶质细胞表达p75， p75缺失导致凋亡的少突胶质细胞数量减少，少突胶质细胞存活率提高。ProNGF可能在体内激活p75，因为来自损伤脊髓的ProNGF诱导p75（+/+）细胞凋亡，而不是培养的p75（-/-）少突胶质细胞凋亡，并且其作用被ProNGF特异性抗体阻断。综上所述，这些数据表明proNGF的作用是通过激活损伤后p75的凋亡机制来消除受损细胞。
The neurotrophin receptor p75 is induced by various injuries to the nervous system, but its role after injury has remained unclear. Here, we report that p75 is required for the death of oligodendrocytes following spinal cord injury, and its action is mediated mainly by proNGF. Oligodendrocytes undergoing apoptosis expressed p75, and the absence of p75 resulted in a decrease in the number of apoptotic oligodendrocytes and increased survival of oligodendrocytes. ProNGF is likely responsible for activating p75 in vivo, since the proNGF from the injured spinal cord induced apoptosis among p75(+/+), but not among p75(-/-), oligodendrocytes in culture, and its action was blocked by proNGF-specific antibody. Together, these data suggest that the role of proNGF is to eliminate damaged cells by activating the apoptotic machinery of p75 after injury.