...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Stem cells and development >Glutamate Increases In Vitro Survival and Proliferation and Attenuates Oxidative Stress-Induced Cell Death in Adult Spinal Cord-Derived Neural Stem/Progenitor Cells via Non-NMDA Ionotropic Glutamate Receptors
【24h】

Glutamate Increases In Vitro Survival and Proliferation and Attenuates Oxidative Stress-Induced Cell Death in Adult Spinal Cord-Derived Neural Stem/Progenitor Cells via Non-NMDA Ionotropic Glutamate Receptors

机译：谷氨酸通过非NMDA离子型谷氨酸受体增加成年脊髓源性神经干细胞/祖细胞中体外存活和增殖并减轻氧化应激诱导的细胞死亡。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Traumatic spinal cord injury (SCI) leads to a cascade of secondary chemical insults, including oxidative stress and glutamate excitotoxicity, which damage host neurons and glia. Transplantation of exogenous neural stem/progenitor cells (NSPCs) has shown promise in enhancing regeneration after SCI, although survival of transplanted cells remains poor. Understanding the response of NSPCs to the chemical mediators of secondary injury is essential in finding therapies to enhance survival. We examined the in vitro effects of glutamate and glutamate receptor agonists on adult rat spinal cord-derived NSPCs. NSPCs isolated from the periventricular region of the adult rat spinal cord were exposed to various concentrations of glutamate for 96 h. We found that glutamate treatment (500 mM) for 96 h significantly increased live cell numbers, reduced cell death, and increased proliferation, but did not significantly alter cell phenotype. Concurrent glutamate treatment (500 mM) in the setting of H2O2 exposure (500 mM) for 10 h increased NSPC survival compared to H2O2 exposure alone. The effects of glutamate on NSPCs were blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor antagonist GYKI-52466, but not by the N-methyl-D-aspartic acid receptor antagonist MK-801 or DL-AP5, or the mGluR3 antagonist LY-341495. Furthermore, treatment of NSPCs with AMPA, kainic acid, or the kainate receptor-specific agonist (RS)-2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl) propanoic acid mimicked the responses seen with glutamate both alone and in the setting of oxidative stress. These findings offer important insights into potential mechanisms to enhance NSPC survival and implicate a potential role for glutamate in promoting NSPC survival and proliferation after traumatic SCI.
机译：创伤性脊髓损伤（SCI）会导致一系列继发性化学损伤，包括氧化应激和谷氨酸兴奋性中毒，这些损伤会损害宿主神经元和神经胶质。外源神经干/祖细胞（NSPC）的移植已显示出增强SCI后再生的希望，尽管移植细胞的存活率仍然很低。了解NSPC对继发性损伤的化学介体的反应对于寻找提高生存率的疗法至关重要。我们检查了谷氨酸和谷氨酸受体激动剂对成年大鼠脊髓源性NSPC的体外作用。从成年大鼠脊髓的脑室周围区域分离的NSPCs暴露于各种浓度的谷氨酸96小时。我们发现，谷氨酸处理（500 mM）96小时可显着增加活细胞数量，减少细胞死亡和增加增殖，但不会显着改变细胞表型。与单独暴露于H2O2相比，在暴露于H2O2（500 mM）10小时的情况下同时进行谷氨酸盐处理（500 mM）可以提高NSPC存活率。谷氨酸对NSPCs的作用被α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）/海藻酸酯受体拮抗剂GYKI-52466阻断，但未被N-甲基-D-天冬氨酸受体阻断拮抗剂MK-801或DL-AP5或mGluR3拮抗剂LY-341495。此外，用AMPA，海藻酸或海藻酸酯受体特异性激动剂（RS）-2-氨基-3-（3-羟基-5-叔丁基异唑基-4-基）丙酸对NSPC的处理模仿了谷氨酸单独和在氧化应激的情况下。这些发现为增强NSPC存活的潜在机制提供了重要见解，并暗示了谷氨酸在促进SCI后促进NSPC存活和增殖中的潜在作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号