TRIM32 affects the recovery of motor function following spinal cord injury through regulating proliferation of glia.
TRIM32 affects the recovery of motor function following spinal cord injury through regulating proliferation of glia.
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TRIM32通过调节胶质细胞增殖影响脊髓损伤后运动功能的恢复
DOI：
10.18632/oncotarget.17492
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发表时间：
2017-07-11
期刊：
影响因子：
--
通讯作者：
Xu RX
中科院分区：
文献类型：
--
作者：
Fu Q;Zou MM;Zhu JW;Zhang Y;Chen WJ;Cheng M;Liu CF;Ma QH;Xu RX
脊髓损伤后轴突再生受到外在环境因素和内在神经机制的双重限制。然而，潜在的分子机制仍不清楚。在本研究中，我们确定三方基序蛋白32（TRIM 32），E3泛素连接酶，这是几乎没有检测到在正常的未受伤的脊髓胶质细胞，表现出强烈的表达在星形胶质细胞和小胶质细胞SCI后。我们进一步观察到TRIM 32的缺乏导致星形胶质细胞和小胶质细胞数量增加，这伴随着两种细胞的增殖增强和白细胞介素（IL）-1和IL-10的分泌增加。SCI后TRIM 32 −/−小鼠脊髓中的轴突再生受损，这表现为皮质脊髓束（CST）纤维到病变部位的距离增加和轴突发芽减少。我们进一步表明，TRIM 32的缺陷导致延迟运动恢复后SCI。因此，TRIM 32是一种新的必需的正性因子，可能通过抑制胶质细胞的增殖来调节脊髓损伤后轴突再生和运动功能的恢复。
Both the extrinsic environmental factors and intrinsic neuronal mechanisms limit the axonal regeneration after spinal cord injury (SCI). However, the underlying molecular mechanisms remain unclear. In the present study, we identify tripartite motif protein 32 (TRIM32), an E3 ubiquitin ligase, which is barely detected in glial cells in the normal uninjured spinal cord, exhibits strong expression in both astrocytes and microglia following SCI. We further observe that deficiency of TRIM32 results in increased numbers of astrocytes and microglia, which is accompanied by enhanced proliferation of both cells and increased secretion of interleukin (IL)-1 and IL-10. The axonal regeneration is impaired in the spinal cord of TRIM32−/− mice following SCI, which is indicated by increased distances of the corticospinal tracts (CST) fiber to the lesion site and less axonal sprouting. We further show that deficiency of TRIM32 results in delay motor recovery following SCI. Therefore, TRIM32 is a novel essential positive factor modulating axonal regeneration and the recovery of motor function following SCI, possibly through suppressing proliferation of glial cells.
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影响因子：
3.4
作者：
Ledeboer, A;Brevé, JJP;Van Dam, AM
通讯作者：
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影响因子：
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影响因子：
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Shioda S
影响因子：
5.2
作者：
Hillje, Anna-Lena;Worlitzer, Maik M. A.;Schwamborn, Jens C.
通讯作者：
Schwamborn, Jens C.