...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >A Transcriptional Roadmap to the Senescence and Differentiation of Human Oral Keratinocytes
【24h】

A Transcriptional Roadmap to the Senescence and Differentiation of Human Oral Keratinocytes

机译：转录路线图的人类口腔角质形成细胞的衰老和分化。

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

Human epithelial cells undergo morphological and molecular changes leading to terminal differentiation and replicative senescence after a finite number of cell divisions during serial subculture. However, the target genes and their functional significance in the senescence and differentiation in normal human oral keratinocytes have been poorly defined. Here, we demonstrated normal human oral keratinocytes transcriptional signature profiling to senescence and differentiation. Using microarray analysis, our findings indicated that the gene expression profiles induced by serial subculture are distinct classes of gene. The greatest number of these altered genes was identified as being related to biological pathways of transport, cell proliferation, cell cycle, defense and immune response, cell death, transcription, apoptosis, and inflammatory response, suggesting that the serial subculture is able to induce a multitude of specific gene expression changes during senescence and differentiation. Several highly upregulated genes (IL-1 beta, S100A8, S100A9, MMP1, MMP9, IL-8, BHLHB2, HES1, and TWIST1) in response to the serial subculture in normal human oral keratinocytes were observed. In vitro and in vivo studies also exhibited a close relationship between senescence and differentiation of primary oral keratinocytes and expression of inflammatory molecules. These results suggest a new approach to determine the biological events underlying the pathogenesis of oral keratinocyte aging.
机译：在连续的继代培养过程中，经过有限次数的细胞分裂后，人类上皮细胞会发生形态和分子变化，从而导致终末分化和复制性衰老。但是，目标基因及其在正常人口腔角质形成细胞衰老和分化中的功能意义尚不清楚。在这里，我们证明了正常的人类口腔角质形成细胞转录特征谱能够衰老和分化。使用微阵列分析，我们的发现表明，连续传代培养诱导的基因表达谱是不同的基因类别。这些改变的基因中最多的是与运输，细胞增殖，细胞周期，防御和免疫反应，细胞死亡，转录，细胞凋亡和炎性反应的生物学途径有关的，这表明该系列继代培养物能够诱导肝癌发生。衰老和分化过程中许多特定的基因表达发生变化。在正常人口腔角质形成细胞中，观察到响应于连续继代培养的几个高度上调的基因（IL-1 beta，S100A8，S100A9，MMP1，MMP9，IL-8，BHLHB2，HES1和TWIST1）。体外和体内研究还显示出衰老与原代口腔角质形成细胞的分化与炎症分子表达之间的密切关系。这些结果提示了一种确定口腔角质形成细胞衰老发病机理的生物学事件的新方法。

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