...
首页> 外文期刊>Cell biology international. >AMP-activated protein kinase is involved in induction of protective autophagy in astrocytes exposed to oxygen-glucose deprivation
【24h】

AMP-activated protein kinase is involved in induction of protective autophagy in astrocytes exposed to oxygen-glucose deprivation

机译:AMP活化的蛋白激酶参与诱导暴露于氧葡萄糖剥夺的星形胶质细胞的保护性自噬

获取原文
获取原文并翻译 | 示例
           

摘要

AMP-activated kinase (AMPK) acts as the intracellular ATP depletion sensor, which detects and limits increases in the AMP/ ATP ratio. AMPK may be significantly activated under stress conditions that deplete cellular ATP levels such as ischemia/ hypoxia or glucose deprivation. Recent studies strongly suggest that AMPK participates in autophagy regulation, but it is not known whether AMPK activated by ischemia regulates autophagy in astrocytes and the consequence of autophagy activation in ischemic astrocytes are unclear. We have investigated the contribution of AMPK to autophagy activation in rat primary astrocyte cultures subjected to ischemia-simulating conditions (combined oxygen glucose deprivation, OGD) and its potential effects on astrocyte damage induced by OGD (1-12 h). The evidence supports the conclusion that AMPK activation at early stages of OGD is involved in induction of protective autophagy in astrocytes. Inhibition of AMPK, either by siAMPKalpha1 or by compound C, significantly attenuated the expression of autophagy-related proteins and decrease of astrocyte viability following OGD. The findings provide additional data about the role of AMPK in ischemic astrocytes and downstream responses that may be involved in OGD-induced protective autophagy.
机译:AMP活化激酶(AMPK)用作细胞内ATP耗尽传感器,其检测和限制在AMP / ATP比率中增加。 AMPK可以在耗尽细胞ATP水平的胁迫条件下显着激活,例如缺血/缺氧或葡萄糖剥夺。最近的研究表明,安培参与自噬调节,但尚不清楚通过缺血激活的AMPK调节星形胶质细胞的自噬,缺血星形胶质细胞中自噬激活的结果尚不清楚。我们研究了AMPK在对缺血模拟条件进行的大鼠原代星形胶质细胞培养物中对自噬激活的贡献(组合氧葡萄糖剥夺,OGD)及其对OGD诱导的星形胶质细胞损伤的潜在影响(1-12小时)。证据支持结论,OGD早期阶段的AMPK活化参与诱导星形胶质细胞的保护性自噬。通过Siampkalpha1或化合物C的AMPK抑制显着抑制了与OGD后的自噬相关蛋白的表达和减少的星形胶质细胞活力。该研究结果提供了有关AMPK在缺血星形胶质细胞和下游反应中可能参与OGD诱导的保护性自噬的额外数据。

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