...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Hyperosmolarity-mediated mitochondrial dysfunction requires Transglutaminase-2 in human corneal epithelial cells.
【24h】

Hyperosmolarity-mediated mitochondrial dysfunction requires Transglutaminase-2 in human corneal epithelial cells.

机译：Hyperosmolarity-mediated线粒体功能障碍需要Transglutaminase-2人类角膜上皮细胞。

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

Hyperosmolar-induced ocular surface cell death is a key mitochondria-mediated event in inflammatory eye diseases. Transglutaminase (TGM)-2, a cross-linking enzyme, is purported to mediate cell death, but its link to mitochondria is unclear. In the cornea, the integrity of the epithelial cells is important for maintaining transparency of the cornea and therefore functional vision. We evaluated the role of TGM-2 and its involvement in hyperosmolarity-stimulated mitochondrial cell death in human corneal epithelial (HCE-T) cells. HCE-T cell lines stably expressing either shRNA targeting TGM-2 (shTG) or scrambled shRNA (shRNA) were constructed. Hyperosmolar conditions reduced viability and increased mitochondrial depolarization in shRNA cells. However, hyperosmolarity failed to induce mitochondrial depolarization to the same extent in shTG cells. Transient overexpression of TGM-2 resulted in very high levels of TGM-2 expression in shTG and shRNA cells. In the case of shTG cells after overexpression of TGM-2, hyperosmolarity induced the same extent of mitochondrial depolarization as similarly treated shRNA cells. Overexpression of TGM-2 also elevated transamidase activity and reduced viability. It also induced mitochondrial depolarization, increased caspase-3/7 and -9 activity, and these increases were partially suppressed by pan-caspase inhibitor Z-VAD-FMK. Corneal epithelial apoptosis via mitochondrial dysfunction after hyperosmolar stimulation is partially dependent on TGM-2. This TGM-2-dependent mechanism occurs in part via caspase-3/7 and -9. Protection against mitochondrial stress in the ocular surface targeting TGM-2 may have important implications in the survival of cells in hyperosmolar stress.
机译：Hyperosmolar-induced眼部表面细胞死亡炎症的关键mitochondria-mediated事件眼睛的疾病。交联酶,是传说中的调解线粒体是细胞死亡,但其链接不清楚。上皮细胞对维护很重要角膜的透明性,因此功能性视力。及其参与hyperosmolarity-stimulated线粒体在人类角膜细胞死亡上皮细胞(HCE-T)。表达要么shRNA针对TGM-2 (shTG)或炒成分(成分)。Hyperosmolar减少生存能力和条件线粒体去极化成分增加细胞。线粒体去极化程度不尽相同在shTG细胞。导致高水平的TGM-2表达式在shTG shRNA细胞。细胞过度TGM-2之后,hyperosmolarity引起相同的程度线粒体去极化是同样的待遇细胞成分。高架transamidase活动和减少生存能力。去极化,增加caspase-3/7和9活动,这些增加部分由Z-VAD-FMK pan-caspase抑制剂抑制。通过线粒体角膜上皮细胞凋亡hyperosmolar刺激后功能障碍部分依赖于TGM-2。通过TGM-2-dependent机制发生在部分caspase-3/7 9。线粒体眼表面的压力针对TGM-2可能具有重要意义hyperosmolar细胞生存的压力。

著录项

相似文献

  • 外文文献
  • 中文文献
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