Brain-derived neurotrophic factor supports facial motoneuron survival after facial nerve transection in immunodeficient mice
Brain-derived neurotrophic factor supports facial motoneuron survival after facial nerve transection in immunodeficient mice
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DOI：
10.1016/j.bbi.2004.07.005
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发表时间：
2005-03-01
影响因子：
15.1
通讯作者：
Jones, KJ
中科院分区：
文献类型：
--
作者：
Serpe, CJ;Byram, SC;Jones, KJ
大量研究表明，损伤后神经营养因子（NTF）可以促进运动神经元的存活。然而，特定 NTF 拯救免疫缺陷小鼠因轴切术引起的死亡的面部运动神经元 (FMN) 的能力尚未得到测试。因此，本研究的一个目标是确定脑源性神经营养因子 (BDNF)（一种已知能够拯救 FMN 免于轴索切断术诱导的死亡的 NTF）是否支持缺乏功能性 T 和 B 淋巴细胞的重组酶激活基因 2 敲除 (RAG-2 KO) 小鼠的 FMN 免遭轴索切断术诱导的死亡。神经生长因子，已被证明对运动神经元的存活没有作用。用作阴性对照。脑源性神经营养因子治疗使 FMN 存活率在术后 4 周 (wpo) 恢复至野生型 (A[T) 对照水平（分别为 80% +/- 1.9、83% +/- 2.4）。本研究的第二个目标是开始阐明面神经轴突切除术后 CD4(+) T 细胞是否产生 NTF。术后 9 天从 WT 小鼠中收集颈部淋巴结，用抗 CD3 重新激活，24 小时后收集上清液。损伤后立即将上清液给予 RAG-2 KO 小鼠，导致 FMN 存活率增加，相当于 WT 对照（分别为 80% +/- 1.4、84% +/- 2.1，4 wpo）。此外，用抗 BDNF 处理的颈部淋巴结上清液减弱了 RAG-2 KO 小鼠 (62% +/- 3.3) 4 wpo 中的 FMN 救援。这些数据支持了这样的假设：CD4(+) T 细胞在靶点重新连接发生之前产生支持运动神经元存活的 NTF。 (C) 2004 Elsevier Inc. 保留所有权利。
Numerous studies have shown that motoneuron survival can be facilitated by neurotrophic factors (NTF) after injury. However, the ability of specific NTF to rescue facial motoneurons (FMN) from axotomy-induced death in immunodeficient mice has not beer, tested. Therefore, one goal of this study was to determine if brain-derived neurotrophic factor (BDNF), an NTF with a known ability to rescue FMN from axotomy-induced death, supports FMN from axotomy-induced death in recombinase activating gene-2 knockout (RAG-2 KO) mice that lack functional T and B lymphocytes. Nerve growth factor, which has been shown not to play a role in motoneuron survival. was used as a negative control. Brain derived neurotrophic factor treatment restored FMN survival to wild-type (A[T) control levels 4 weeks post-operative (wpo) (80% +/- 1.9. 83% +/- 2.4, respectively). The second goal of this study was to begin to elucidate if CD4(+) T cells produce NTF after facial nerve axotomy, Cervical lymph nodes were collected from WT mice 9 days post-operative, re-activated with anti-CD3 and supernatant collected 24 h later. Immediately after injury, the supernatant was administered to RAG-2 KO mice leading to an increase in FMN survival equivalent to WT controls (80% +/- 1.4. 84% +/- 2.1, respectively, 4 wpo). In addition, cervical lymph node supernatant treated with anti-BDNF attenuated FMN rescue in RAG-2 KO mice (62% +/- 3.3) 4 wpo. These data lend support to the hypothesis that CD4(+) T cells produce NTF that support motoneuron survival before target reconnection occurs. (C) 2004 Elsevier Inc. All rights reserved.