...
首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Profiling of BoNT/C3-reversible gene expression induced by lysophosphatidic acid: ephrinB1 gene up-regulation underlying neuropathic hyperalgesia and allodynia.
【24h】

Profiling of BoNT/C3-reversible gene expression induced by lysophosphatidic acid: ephrinB1 gene up-regulation underlying neuropathic hyperalgesia and allodynia.

机译:溶血磷脂酸诱导的BoNT / C3可逆基因表达的概况分析:ephrinB1基因上调潜在的神经性痛觉过敏和异常性疼痛。

获取原文
获取原文并翻译 | 示例
           

摘要

Lysophosphatidic acid (LPA) signaling, through LPA(1) receptor and its downstream RhoA, has been reported to initiate nerve injury-induced neuropathic pain. In the present study, we performed gene expression profiling of the dorsal root ganglion (DRG) to identify genes induced by intrathecal injection of LPA in a botulinum toxin C3 (BoNT/C3)-reversible manner. We selected and functionally characterized ephrinB1 from 82 identified genes as a potential gene involved in pain transmission, since ephrinB1 is implicated to modulate N-methyl-d-aspartate (NMDA) receptor functions in spinal pain transmission. The LPA-induced and BoNT/C3-reversible ephrinB1 gene expression was confirmed by quantitative real-time PCR. Furthermore, treatments with an antisense oligodeoxynucleotide for ephrinB1 largely abolished the LPA-induced thermal hyperalgesia and allodynia in response to mechanical or Abeta-fiber-mediated electrical stimuli on day 1 after the injection. In addition, intrathecal treatment with a soluble ligand, ephrinB1-Fc, caused similar neuropathic pain-like behaviors in a manner that was reversible by the NMDA receptor antagonist MK-801. These results suggest that ephrinB1 plays a crucial role in LPA-induced neuropathic pain. In addition, the present study may provide a new strategy to identify unique neuropathic pain-related genes.
机译:据报道,通过LPA(1)受体及其下游RhoA的溶血磷脂酸(LPA)信号可引发神经损伤引起的神经性疼痛。在本研究中,我们进行了背根神经节(DRG)的基因表达谱分析,以鉴定鞘内注射LPA以肉毒杆菌毒素C3(BoNT / C3)可逆方式诱导的基因。我们从82个已鉴定的基因中选择了ephrinB1并进行了功能表征,将其作为疼痛传递的潜在基因,因为ephrinB1参与了脊髓疼痛传递中的N-甲基-d-天冬氨酸(NMDA)受体功能的调控。 LPA诱导和BoNT / C3可逆的ephrinB1基因表达已通过实时定量PCR证实。此外,在注射后第1天,对机械或Abeta纤维介导的电刺激作出反应,使用针对ephrinB1的反义寡聚脱氧核苷酸治疗可大大消除LPA引起的热痛觉过敏和异常性疼痛。另外,鞘内用可溶性配体ephrinB1-Fc的治疗以类似的神经病理性疼痛样行为,其方式可被NMDA受体拮抗剂MK-801逆转。这些结果表明,ephrinB1在LPA诱发的神经性疼痛中起关键作用。另外,本研究可能提供一种鉴定独特的神经性疼痛相关基因的新策略。

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