首页> 外文会议>International Symposium on Molecular Mechanism and Epochal Therapeutics for Ischemic Stroke and Dementia >Hypoxic induction of vascular endothelial growth factor is impaired in the spinal cord of the mice with mutant human SOD1 gene
【24h】

Hypoxic induction of vascular endothelial growth factor is impaired in the spinal cord of the mice with mutant human SOD1 gene

机译:血管内皮生长因子的缺氧诱导在突变人SOD1基因的小鼠的脊髓中受损

获取原文

摘要

We examined the induction of vascular endothelial growth factor (VEGF) in the G93 A superoxide dismutase (SOD)l-mutant mice exposed to systemic hypoxia. Generally, baseline expression of VEGF in the spinal cord was increased in the SOD 1-mutant mice compared with wild-type littermates. VEGF expression in the mutant mice was hardly induced by hypoxia, in contrast to the wild-type littermates where approximately 9-fold increase in VEGF expression was observed, indicating that the response of VEGF to hypoxia is impaired in the SOD 1-mutant mice. Our results suggest that the impaired response to hypoxia might be part of precipitating factors for motor neuron death in the SOD 1-mutant mice.
机译:我们研究了G93中的血管内皮生长因子(VEGF)的诱导,其暴露于全身缺氧的超氧化物歧化酶(SOD)L-突变小鼠。通常,与野生型凋落物相比,SOD 1-突变小鼠中VEGF在脊髓中的基线表达增加。与缺氧诱导突变小鼠的VEGF表达,与观察到VEGF表达的大约9倍增加的野生型凋落物相反,表明在SOD 1-突变小鼠中损害VEGF至缺氧的响应。我们的研究结果表明,对缺氧的反应受损可能是SOD 1-突变小鼠的运动神经元死亡的沉淀因子的一部分。

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