• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Reduced cerebral injury in CRH-R1 deficient mice after focal ischemia: a potential link to microglia and atrocytes that express CRH-R1.
【24h】

Reduced cerebral injury in CRH-R1 deficient mice after focal ischemia: a potential link to microglia and atrocytes that express CRH-R1.

机译：减少局灶性缺血后CRH-R1缺陷小鼠的脑损伤：与表达CRH-R1的小胶质细胞和星形胶质细胞的潜在联系。

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

Corticotropin releasing hormone (CRH) and its family of related peptides are involved in regulating physiologic responses to multiple stressors, including stroke. Although CRH has been implicated in the exacerbation of injury after stroke, the mechanism remains unclear. After ischemia, both excitotoxic damage and inflammation contribute to the pathology of stroke. CRH is known to potentiate excitotoxic damage in the brain and has been shown to modulate inflammatory responses in the periphery. Here the present authors examine the relative contribution of the two known CRH receptors, CRH-R1 and CRH-R2, to ischemic injury using CRH receptor knockout mice. These results implicate CRH-R1 as the primary mediator of ischemic injury in this mouse model of stroke. In addition, the authors examine a potential role for CRH in inflammatory injury after stroke by identifying functional CRH receptors on astrocytes and microglia, which are cells that are known to be involved in brain inflammation. By single cell PCR,the authors show that microglia and astrocytes express mRNA for both CRH-R1 and CRH-R2. However, CRH-R1 is the primary mediator of cAMP accumulation in response to CRH peptides in these cells. The authors suggest that astrocytes and microglia are cellular targets of CRH, which could serve as a link between CRH and inflammatory responses in ischemic injury via CRH-R1.
机译：促肾上腺皮质激素释放激素（CRH）及其相关肽家族参与调节对多种应激源（包括中风）的生理反应。尽管CRH与中风后的损伤加重有关，但其机制仍不清楚。缺血后，兴奋性中毒损害和炎症都会导致中风的病理。已知CRH会增强大脑中的兴奋性毒性损伤，并已显示出它可以调节周围的炎症反应。在这里，作者研究了使用CRH受体敲除小鼠的两种已知CRH受体CRH-R1和CRH-R2对缺血性损伤的相对贡献。这些结果暗示CRH-R1是这种中风小鼠模型中缺血性损伤的主要介质。此外，作者通过鉴定星形胶质细胞和小胶质细胞上的功能性CRH受体来检查CRH在中风后炎症损伤中的潜在作用，这些受体是已知参与脑部炎症的细胞。通过单细胞PCR，作者显示小胶质细胞和星形胶质细胞表达CRH-R1和CRH-R2的mRNA。但是，CRH-R1是这些细胞中响应CRH肽的cAMP积累的主要介质。作者认为，星形胶质细胞和小胶质细胞是CRH的细胞靶标，在CRH-R1引起的缺血性损伤中，CRH和炎症反应之间可能存在联系。

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