...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Chronic high glucose and insulin stimulate bone‐marrow stromal cells adipogenic differentiation in young spontaneously hypertensive rats
【24h】

Chronic high glucose and insulin stimulate bone‐marrow stromal cells adipogenic differentiation in young spontaneously hypertensive rats

机译：慢性高葡萄糖和胰岛素刺激骨骨髓基质细胞脂肪形成的年轻自发分化高血压大鼠

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

We evaluated whether genetic predisposition is sufficient to induce changes due to chronic high glucose (HG; 25?mmol/L) in the presence or absence of insulin (HGI; 10?μg/ml) on osteogenic differentiation and markers in bone‐marrow mesenchymal stem cells (BMSCs) from young Wistar (WBMSCs) and spontaneous hypertensive rats (SBMSCs) without hypertension. HG suppressed osteogenic differentiation in both the strains, observed by mineralization inhibition and decreased levels of the osteogenic markers Runx2 , osterix , osteopontin , and bone sialoprotein , compared to osteogenic medium (OM) cells. In WBMSCs, the effects of HG were associated with the down regulation of ERK1/2 and up regulation of p38 activities; however, HGI did not revert the effects of HG on MAPK activities. Moreover, HG did not affect MAPK signaling in SBMSCs compared to that in OM. HGI increased mineralization in WBMSCs compared to that in OM, but not in SBMSCs. High expression of peroxisome proliferator‐activated receptor‐gamma and glucose transporter type 4 in OM could be related with the predisposition to adipogenic differentiation noted in SBMSCs and was confirmed by emergence of adipocyte‐like cells by HGI treatment. Downregulation of p38 and upregulation of JNK activities were observed in both BMSCs treated with HGI compared to those treated by HG. Ma (osmotic control) also suppressed osteogenic differentiation in both the strains. In conclusion, we demonstrated that SBMSCs from young spontaneous hypertensive rats, without hypertension but with genetic and epigenetic predisposition, exhibited decreased osteoblastic differentiation under HG and HGI did not revert the effects of HG in SBMSCs but increased adipogenic differentiation.
机译：我们评估是否遗传倾向由于慢性高足以引起变化葡萄糖(HG;缺乏胰岛素(HGI;负责分化和骨标记的骨髓间充质干细胞(bmsc)年轻的纯种(WBMSCs)和自发高血压大鼠(SBMSCs)没有高血压。成骨分化的菌株,观察到矿化抑制成骨的标记Runx2的水平下降osterix,骨桥蛋白和骨涎蛋白,与成骨的介质(OM)细胞。WBMSCs, HG的影响有关ERK1/2监管和监管人们的活动;HG MAPK活动的影响。在SBMSCs HG并不影响MAPK信号而,在OM。矿化在WBMSCs相比,在OM,但不是在SBMSCs。扩散者优先激活受体γ和葡萄糖OM运输机类型4可能相关脂肪形成的分化的倾向指出SBMSCs和证实了崛起脂肪细胞类细胞HGI治疗负责。Downregulation p38和upregulation物活动是观察综合治疗马HGI相比被HG负责。(渗透控制)也抑制成骨的分化的压力。结论,我们证明了SBMSCs从年轻的自发性高血压大鼠,没有高血压,但遗传和表观遗传倾向,表现出成骨细胞的减少分化在HG HGI不负责恢复HG SBMSCs但增加的影响脂肪形成的分化。

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