Accelerated Nerve Regeneration in Mice by upregulated expression of interleukin (IL) 6 and IL-6 receptor after trauma.
Accelerated Nerve Regeneration in Mice by upregulated expression of interleukin (IL) 6 and IL-6 receptor after trauma.
复制标题
创伤后，通过上调白介素（IL）6和IL-6受体的表达来加速小鼠的神经再生。
DOI：
10.1084/jem.183.6.2627
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发表时间：
1996-06-01
影响因子：
15.3
通讯作者：
Taga, T
中科院分区：
文献类型：
--
作者：
Hirota, H;Kiyama, H;Kishimoto, T;Taga, T
在这项研究中，我们旨在研究白细胞介素6 （IL-6）及其受体（IL-6R）在体内周围神经再生中的作用。我们首先观察到，通过同时添加IL-6和可溶性IL-6R (sIL-6R)，培养的小鼠胚胎背根神经节表现出显著的神经突延伸，IL-6R是一种已知与信号转导受体成分gp130相互作用并激活的复合物。结扎损伤成年小鼠舌下神经后，病变部位的雪旺细胞和脑干舌下神经元细胞体中对IL-6的免疫反应性上调。在后者中，也观察到对IL-6R的免疫反应性上调。抗il - 6r抗体明显延缓舌下神经在体内的再生。令人惊讶的是，与非转基因小鼠相比，在同时表达IL-6和IL-6R的转基因小鼠中实现了轴突切除神经的加速再生。这些结果提示IL- 6信号可能在体内创伤后神经再生中起重要作用。
In this study we aimed to examine a role for interleukin 6 (IL-6) and its receptor (IL-6R) in peripheral nerve regeneration in vivo. We first observed that cultured mouse embryonic dorsal root ganglia exhibited dramatic neurite extension by simultaneous addition of IL-6 and soluble IL-6R (sIL-6R), a complex that is known to interact with and activate a signal transducing receptor component, gp130. After injury in the hypoglossal nerve in adult mice by ligation, immunoreactivity to IL-6 was upregulated in Schwann cells at the lesional site as well as in the cell bodies of hypoglossal neurons in the brain stem. In the latter, upregulation of the immunoreactivity to IL-6R was also observed. Regeneration of axotomized hypoglossal nerve in vivo was significantly retarded by the administration of anti-IL-6R antibody. Surprisingly, accelerated regeneration of the axotomized nerve was achieved in transgenic mice constitutively expressing both IL-6 and IL-6R, as compared with nontransgenic controls. These results suggest that the IL- 6 signal may play an important role in nerve regeneration after trauma in vivo.
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影响因子：
16.2
作者：
BAZAN, JF
通讯作者：
BAZAN, JF
影响因子：
3.3
作者：
FABRY, Z;FITZSIMMONS, KM;HART, MN
通讯作者：
HART, MN
DOI：
10.1073/pnas.92.11.4862
发表时间：
1995-05-23
影响因子：
11.1
作者：
HIROTA, H;YOSHIDA, K;TAGA, T
通讯作者：
TAGA, T
影响因子：
3.4
作者：
KIEFER, R;LINDHOLM, D;KREUTZBERG, GW
通讯作者：
KREUTZBERG, GW
影响因子：
56.9
作者：
MITSUMOTO, H;IKEDA, K;LINDSAY, RM
通讯作者：
LINDSAY, RM