...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>International journal of molecular medicine >miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways
【24h】

miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways

机译：miR-214抑制骨髓间充质干细胞的成骨分化，这些作用是通过抑制JNK和p38途径介导的

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

In this study, we sought to investigate the expression of microRNA?(miR)-214 on the osteogenic differentiation of bone marrow?derived mesenchymal stem cells?(BMSCs) and explore the possible underlying mechanisms. We found that the overexpression of miR?214 effectively promoted the adipocyte differentiation of BMSCs in?vitro, reduced alkaline phosphatase?(ALP) activity and the gene expression of collagen type?I?(Col?I), osteocalcin?(OCN) and osteopontin?(OPN) in the BMSCs. We further found that the overexpression of miR?214 suppressed the protein expression of fibroblast growth factor?(FGF), phosphorylated c?Jun N-terminal kinase?(p-JNK) and phosphorylated p38?(p-p38) in the BMSCs. The downregulation of miR?214 promoted the osteogenic differentiation of BMSCs, and increased ALP activity and Col?I, OCN and OPN gene expression in the BMSCs. It also increased FGF p-JNK and p-p38 protein expression in the BMSCs. The use of JNK inhibitor?(SP600125) enhanced the inhibitory effects of miR?214 overexpression on osteogenic differentiation, ALP activity, and Col?I, OCN and OPN gene expression in the BMSCs. Lastly, the use of p38 inhibitor?(SB202190) also enhanced the inhibitory effects of miR?214 overexpression on ALP activity, and Col?I, OCN and OPN gene expression in the BMSCs. These results provide a mechanism responsible for the suppressive effects of miR?214 on the osteogenic differentiation of BMSCs involving the inhibition of the JNK and p38 pathways.
机译：在这项研究中，我们试图研究microRNA？（miR）-214在骨髓源性间充质干细胞？（BMSCs）的成骨分化中的表达，并探讨可能的潜在机制。我们发现miR？214的过表达有效促进了BMSCs的脂肪细胞体外分化，降低了碱性磷酸酶？（ALP）活性以及？I？型胶原（Col？I），骨钙蛋白？（OCN）和骨髓间质干细胞中的骨桥蛋白？（OPN）。我们还发现，miRα214的过表达抑制了BMSCs中成纤维细胞生长因子β（FGF），磷酸化的cβJunN末端激酶β（p-JNK）和磷酸化的p38β（p-p38）的蛋白表达。 miR？214的下调促进了BMSCs的成骨分化，并增加了BMSCs中的ALP活性和Col？I，OCN和OPN基因表达。它还增加了BMSCs中FGF p-JNK和p-p38蛋白的表达。 JNK抑制剂？（SP600125）的使用增强了miR？214过表达对BMSCs成骨分化，ALP活性以及Col？I，OCN和OPN基因表达的抑制作用。最后，使用p38抑制剂α（SB202190）还增强了miRα214过表达对BMSC中ALP活性以及ColαI，OCN和OPN基因表达的抑制作用。这些结果提供了一种机制，该机制负责miRα214对BMSC的成骨分化的抑制作用，涉及对JNK和p38途径的抑制。

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