首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Adrenoreceptor-coupled signal-transduction mechanisms mediating lymphocyte apoptosis induced by endogenous catecholamines.
【24h】

Adrenoreceptor-coupled signal-transduction mechanisms mediating lymphocyte apoptosis induced by endogenous catecholamines.

机译:肾上腺素耦合信号转导机制介导内源性儿茶素诱导的淋巴细胞凋亡。

获取原文
获取原文并翻译 | 示例
           

摘要

Our previous work has shown that lymphocytes synthesize catecholamines (CAs) and the endogenous CAs accelerate apoptosis of concanavalin A (Con A)-activated lymphocyte. Here, we explored the involvement of adrenoreceptors (ARs) and signal molecules coupled to the ARs in the endogenous CA-mediated modulation of lymphocyte apoptosis. Pargyline, an inhibitor of CA degradation, up-regulated the expression of cleaved caspase-3 protein and increased the number of apoptotic cells. Antagonists of alpha(1)-ARs and beta(2)-ARs, not antagonists of alpha(2)-ARs or beta(1)-ARs, blocked these effects of pargyline. The facilitating effects of pargyline on lymphocyte apoptosis were mimicked by activators of adenylate cyclase and PKC, but reversed by inhibitors of PKA, PLC and PKC. Pargyline-stimulated CREB activation and Smac/DIABLO expression were prevented by the inhibitors of PKA, PLC and PKC. These results imply that endogenous CA-induced lymphocyte apoptosis is mediated by cAMP-PKA- and PLC-PKC-linked CREB-Smac/DIABLO pathways coupled with alpha(1)-ARs and beta(2)-ARs.
机译:我们以前的作品表明,淋巴细胞合成儿茶酚胺(CAS)和内源CAS加速诱变淋巴糊糊剂的凋亡凋亡。在这里,我们探讨了肾上腺菌属(ARS)和信号分子在内源性Ca介导的淋巴细胞凋亡调节中偶联的信号分子。 Pargyline,Ca降解的抑制剂,上调切割的caspase-3蛋白的表达并增加凋亡细胞的数量。 α(1)-AR和β(2)-AR的拮抗剂,而不是α(2)-AR或β(1)-AR的拮抗剂,阻断了pargyline的这些作用。 Pargyline对淋巴细胞凋亡的促进效果被腺苷酸环酶和PKC的活化剂模仿,但通过PKA,PLC和PKC的抑制剂反转。通过PKA,PLC和PKC的抑制剂防止了Pargyline刺激的CREB活化和SMAC /暗黑破坏瘤表达。这些结果意味着内源性Ca诱导的淋巴细胞凋亡由CAMP-PKA-和PLC-PKC连接的CREB-SMAC /暗黑破坏神途径与α(1)-ARS和β(2)-AR介导。

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