...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell cycle >Silencing of RB1 and RB2/P130 during adipogenesis of bone marrow stromal cells results in dysregulated differentiation
【24h】

Silencing of RB1 and RB2/P130 during adipogenesis of bone marrow stromal cells results in dysregulated differentiation

机译：骨髓基质细胞成脂过程中RB1和RB2 / P130的沉默导致分化失调

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

Bone marrow adipose tissue (BMAT) is different from fat found elsewhere in the body, and only recently have some of its functions been investigated. BMAT may regulate bone marrow stem cell niche and plays a role in energy storage and thermogenesis. BMAT may be involved also in obesity and osteoporosis onset. Given the paramount functions of BMAT, we decided to better clarify the human bone marrow adipogenesis by analyzing the role of the retinoblastoma gene family, which are key players in cell cycle regulation. Our data provide evidence that the inactivation of RB1 or RB2/P130 in uncommitted bone marrow stromal cells (BMSC) facilitates the first steps of adipogenesis. In cultures with silenced RB1 or RB2/P130, we observed an increase of clones with adipogenic potential and a higher percentage of cells accumulating lipid droplets. Nevertheless, the absence of RB1 or RB2/P130 impaired the terminal adipocyte differentiation and gave rise to dysregulated adipose cells, with alteration in lipid uptake and release. For the first time, we evidenced that RB2/P130 plays a role in bone marrow adipogenesis. Our data suggest that while the inactivation of retinoblastoma proteins may delay the onset of last cell division and allow more BMSC to be committed to adipocyte, it did not allow a permanent cell cycle exit, which is a prerequisite for adipocyte terminal maturation.
机译：骨髓脂肪组织（BMAT）与体内其他地方的脂肪不同，只是最近才对其某些功能进行了研究。 BMAT可能调节骨髓干细胞的生态位，并在能量存储和生热中起作用。 BMAT也可能与肥胖和骨质疏松症发作有关。鉴于BMAT的最重要功能，我们决定通过分析视网膜母细胞瘤基因家族的作用来更好地阐明人类骨髓的脂肪形成，这是细胞周期调控的关键因素。我们的数据提供了证据，表明未定型的骨髓基质细胞（BMSC）中RB1或RB2 / P130的失活促进了脂肪形成的第一步。在带有沉默的RB1或RB2 / P130的培养物中，我们观察到具有成脂潜能的克隆数量增加，并且积累脂质滴的细胞百分比更高。然而，缺乏RB1或RB2 / P130会损害最终的脂肪细胞分化，并导致脂肪细胞失调，从而改变脂质的摄取和释放。我们首次证明RB2 / P130在骨髓脂肪形成中起作用。我们的数据表明，尽管视网膜母细胞瘤蛋白失活可能会延迟最后一次细胞分裂的发生并允许更多的BMSC进入脂肪细胞，但它不允许永久的细胞周期退出，这是脂肪细胞末端成熟的前提。

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