...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Acta Pharmacologica Sinica >Inhibition of ATP-induced calcium influx in HT4 cells by glucocorticoids: involvement of protein kinase A
【24h】

Inhibition of ATP-induced calcium influx in HT4 cells by glucocorticoids: involvement of protein kinase A

机译：糖皮质激素抑制ATP诱导的HT4细胞钙内流：参与蛋白激酶A

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

Aim: In our previous observations, adenosine triphosphate ( ATP ) was found to evoke immediate elevations in intracellular free calcium concentration ( [ Ca ~( 2+ ) ]_i ) in HT4 neuroblastoma cells of mice. We tried to see if a brief pretreatment of glucocorticoids could inhibit the Ca~( 21 ) response and reveal the underlying signaling mechanism. Methods: Measurement of [ Ca~( 21 ) ]_i ; was carried out using the dual-wavelength fluorescence method with Fura-2 as the indicator. Results: Pre-incubation of HT4 cells for 5 min with corticosterone ( B ) or bovine serum albumin conjugated corticosterone ( B-BSA ) inhibited the peak [ Ca~(2+) ]_i increments in a concentration-dependent manner. Cortisol and dexamethasone had a similar action, while deoxycorticosterone and cholesterol were ineffective. Both extracellular Ca~( 2+ ) influx and internal Ca~( 2+ ) release contributed to ATP-induced [ Ca( 2+ ) ] _ i elevation. The brief treatment with only B attenuated Ca~( 2+ ) influx. Furthermore, the [ Ca ( 2+ ) ]_i elevation induced by the P2X receptor agonist adenosine 5'-(β,γ-methylene) triphosphate ( β,γ-meATP ) was also suppressed. The rapid inhibitory effect of B can be reproduced by forskolin 1 mmol/L and blocked by H89 20 mmol/L. Neither nuclear glucocorticoid receptor antagonist mifepristone nor protein kinase C inhibitors influenced the rapid action of B. Conclusion: Our results suggest that glucocorticoids modulate P2X receptor-medicated Ca~( 2+ ) influx through a membrane-initiated, non-genomic and PKA-dependent pathway in HT4 cells.
机译：目的：在我们先前的观察中，发现三磷酸腺苷（ATP）引起小鼠HT4神经母细胞瘤细胞的细胞内游离钙浓度（[Ca〜（2+）] _i）立即升高。我们试图观察糖皮质激素的简短预处理是否可以抑制Ca〜（21）反应并揭示潜在的信号传导机制。方法：测量[Ca〜（21）] _ i；使用Fura-2作为指示剂的双波长荧光法进行。结果：HT4细胞与皮质酮（B）或牛血清白蛋白缀合的皮质酮（B-BSA）预孵育5分钟，以浓度依赖的方式抑制峰[Ca〜（2+）] _i增量。皮质醇和地塞米松具有相似的作用，而脱氧皮质酮和胆固醇无效。细胞外Ca〜（2+）内流和内部Ca〜（2+）释放均导致ATP诱导的[Ca（2+）] _ i升高。仅用B减弱Ca〜（2+）流入量的短暂治疗。此外，还抑制了由P2X受体激动剂腺苷5'-（β，γ-亚甲基）三磷酸腺苷（β，γ-meATP）引起的[Ca（2 +）] _ i升高。 B的快速抑制作用可以用1 mmol / L的毛喉素来再现，而用20 mmol / L的H89可以阻止。核糖皮质激素受体拮抗剂米非司酮或蛋白激酶C抑制剂均不影响B的快速作用。结论：我们的结果表明，糖皮质激素通过膜启动，非基因组和PKA依赖性调节P2X受体介导的Ca〜（2+）内流。 HT4细胞中的信号通路。

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