...
首页> 外文期刊>Toxicology in vitro: an international journal published in association with BIBRA >MiR-122 partly mediates the ochratoxin A-induced GC-2 cell apoptosis
【24h】

MiR-122 partly mediates the ochratoxin A-induced GC-2 cell apoptosis

机译:MiR-122部分介导曲霉毒素A诱导的GC-2细胞凋亡

获取原文
获取原文并翻译 | 示例

摘要

Ochratoxin A (OTA) is a mycotoxin which has been shown to be nephrotoxic, hepatotoxic, and immunotoxic to animals, and mainly exists in the mildew grain. MicroRNAs (miRNAs) regulate a wide variety of cellular processes. However, the toxic effects of OTA on the germ cell and whether miRNAs mediate the effects of OTA-induced GC-2 cell apoptosis are still not clear. In the present study, OTA treatment resulted in a dose-dependent increase apoptosis in GC-2 cells. MiR-122 was increased in the OTA-treated GC-2 cells. It showed that Bcl-w was down-regulated after arA treatment, and caspase-3 was obviously activated. cyclin Gi (CCNG1) was significantly decreased, and inversely the expression of p53 was increased. Inhibition of miR-122 partly relieved the OTA-induced GC-2 cell apoptosis. These results indicate that OTA induces GC-2 cell apoptosis by causing the increase of caspase-3 activity and that miR-122 partly mediates the OTA-induced cell apoptosis. (C) 2015 Elsevier Ltd. All rights reserved.
机译:ch曲霉毒素A(OTA)是一种霉菌毒素,已证明对动物具有肾毒性,肝毒性和免疫毒性,主要存在于霉菌谷物中。微小RNA(miRNA)调节多种细胞过程。然而,尚不清楚OTA对生殖细胞的毒性作用以及miRNA是否介导OTA诱导的GC-2细胞凋亡的作用。在本研究中,OTA处理导致GC-2细胞凋亡呈剂量依赖性增加。在OTA处理的GC-2细胞中,MiR-122含量增加。结果表明,arA处理后Bcl-w被下调,caspase-3明显被激活。细胞周期蛋白Gi(CCNG1)显着降低,而p53的表达反而升高。 miR-122的抑制部分缓解了OTA诱导的GC-2细胞凋亡。这些结果表明,OTA通过引起caspase-3活性增加而诱导GC-2细胞凋亡,而miR-122部分介导了OTA诱导的细胞凋亡。 (C)2015 Elsevier Ltd.保留所有权利。

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