...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Human and Experimental Toxicology >Upregulated miR-29c suppresses silica-induced lung fibrosis through the Wnt/-catenin pathway in mice
【24h】

Upregulated miR-29c suppresses silica-induced lung fibrosis through the Wnt/-catenin pathway in mice

机译：上调的miR-29c通过小鼠的Wnt / -catenin途径抑制二氧化硅诱导的肺纤维化

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

Silicosis is an irreversible lung disease resulting from long-term inhalation of occupational dust containing silicon dioxide. However, the pathogenesis of silicosis has not been clearly understood yet. Accumulating evidence suggests that miR-29 may have a significant anti-fibrotic capacity, meanwhile it may relate to Wnt/-catenin pathway. The purpose of this study was to discuss the role of miR-29 in the progression of silicosis. A lentiviral vector was constructed, named Lv-miR-29c, which was overexpressing miR-29c. In vivo, intratracheal treatment with Lv-miR-29c significantly increased expression of miR-29c, and reduced expression of -catenin, matrix metalloproteinase (MMP)-2, and MMP-9 in the lung and levels of transforming growth factor-beta 1 (TGF-1) and interleukin-6 (IL-6) in bronchoalveolar lavage fluid, and notably attenuated pulmonary fibrosis as evidenced by hydroxyproline content in silica-administered mice. These results indicated that miR-29c inhibited the development of silica-induced lung fibrosis. Thus, miR-29c may be a candidate target for silicosis treatment via its regulation of the Wnt/-catenin pathway.
机译：矽肺是一种不可逆的肺部疾病，由长期吸入含有二氧化硅的职业性粉尘引起。然而，矽肺的发病机制尚不清楚。越来越多的证据表明，miR-29可能具有显著的抗纤维化能力，同时它可能与Wnt/-catenin途径有关。本研究的目的是探讨miR-29在矽肺进展中的作用。构建了一个名为Lv-miR-29c的慢病毒载体，该载体过度表达miR-29c。在体内，Lv-miR-29c气管内治疗显著增加了肺组织中miR-29c的表达，降低了-连环蛋白、基质金属蛋白酶（MMP）-2和MMP-9的表达，以及支气管肺泡灌洗液中转化生长因子β1（TGF-1）和白细胞介素-6（IL-6）的水平，二氧化硅给药小鼠体内的羟脯氨酸含量证明，显著减轻了肺纤维化。这些结果表明miR-29c抑制二氧化硅诱导的肺纤维化的发展。因此，miR-29c可能通过调节Wnt/-catenin途径成为矽肺治疗的候选靶点。

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