• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Neuronal expression and regulation of rat inhibitor of apoptosis protein-2 by kainic acid in the rat brain.
【24h】

Neuronal expression and regulation of rat inhibitor of apoptosis protein-2 by kainic acid in the rat brain.

机译：海藻酸在大鼠脑中对细胞凋亡蛋白2抑制剂的神经元表达和调控。

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

Inhibitors of apoptosis proteins (IAPs) define a protein family with the ability to counteract cell death by the inhibition of different caspases activated during apoptosis. These proteins are present in different cells, however, the function and roles of IAPs in brain tissue are not fully understood. We report here that RIAP-2, the rat homologue of human cIAP-1/HIAP-2, is expressed in different areas of rat brain as shown by in situ hybridization and immunohistochemistry. Brain regions with relatively high expression of RIAP-2 mRNA included cortex, cerebellum and different subregions of rat hippocampus. Double labelling using a specific anti-RIAP antibody and markers for neurons and glial cells, showed that RIAP-2 is predominantly expressed by nerve cells. Kainic acid treatment, which induces seizures, transiently up-regulated RIAP-2 mRNA levels in cerebral cortex, in the CA1 and dentate gyrus regions of hippocampus, which returned to normal levels at 24 h. However in the CA3 region, RIAP-2 mRNA was decreased at 6 h following an early up-regulation. This region contains neurons particularly vulnerable to kainic acid induced cell degeneration. The decrease in RIAP-2 following kainic acid was also observed using immunohistochemistry. RIAP-2 protein did not colocalize with TUNEL labelling present in cells undergoing cell death. The results show that in the adult rat brain RIAP-2 is expressed mainly by neurons, and that the levels are regulated by kainic acid, which activates glutamate receptors. The decrease in RIAP-2 in specific neuronal populations may contribute to cell degeneration in vulnerable brain regions observed after kainic acid treatment.
机译：凋亡蛋白抑制剂（IAP）定义了一个蛋白家族，该蛋白家族具有通过抑制凋亡过程中激活的不同胱天蛋白酶来抵消细胞死亡的能力。这些蛋白质存在于不同的细胞中，但是，IAP在脑组织中的功能和作用尚不完全清楚。我们在这里报告RIAP-2，人类cIAP-1 / HIAP-2的大鼠同源物，在大鼠大脑的不同区域表达，如原位杂交和免疫组织化学所示。 RIAP-2 mRNA表达相对较高的大脑区域包括皮质，小脑和大鼠海马的不同亚区域。使用特定的抗RIAP抗体和神经元和神经胶质细胞标记进行的双重标记显示RIAP-2主要由神经细胞表达。海藻酸治疗可引起癫痫发作，海马CA1区和齿状回区域的大脑皮层RIAP-2 mRNA瞬时上调，并在24小时恢复正常水平。然而，在CA3区域，RIAP-2 mRNA在早期上调后6小时下降。该区域包含特别容易受到海藻酸诱导的细胞变性的神经元。用免疫组织化学还观察到海藻酸后RIAP-2的减少。 RIAP-2蛋白与经历细胞死亡的细胞中存在的TUNEL标记不共定位。结果表明，成年大鼠大脑中的RIAP-2主要由神经元表达，其水平受海藻酸调节，后者可激活谷氨酸受体。特定神经元群体中RIAP-2的减少可能导致海藻酸治疗后观察到的脆弱脑区域细胞变性。

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