• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell biology international. >HIV-1 p55-gag protein induces senescence of human bone marrow mesenchymal stem cells and reduces their capacity to support expansion of hematopoietic stem cells in vitro
【24h】

HIV-1 p55-gag protein induces senescence of human bone marrow mesenchymal stem cells and reduces their capacity to support expansion of hematopoietic stem cells in vitro

机译：HIV-1 P55-GAG蛋白诱导人骨髓间充质干细胞的衰老，降低了它们在体外支持造血干细胞的膨胀的能力

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

Patients with human immunodeficiency virus-1 (HIV-1) infection often present with hematopoietic failure. As the important hematopoietic support cells in the bone marrow (BM), the BM mesenchymal stem cells (BMSCs) can be impacted by HIV proteins that are released by infected cells within BM. In this study, we tested whether HIV protein p55-gag could induce senescence of BMSCs and reduce their capacity to support expansion of hematopoietic stem cells in vitro. BMSCs were chronically treated with p55-gag (BMSCgag) for up to 20 days, and their proliferative activity and senescence makers were compared to nontreated cells (BMSCcon). Then, we analyzed the hematopoietic support function of BMSCcon and BMSCgag by determining cellular proliferation, colony-forming ability, and primitive hematopoietic populations of hematopoietic progenitors grown on the BMSCs. In addition, we compared the gene expression patterns for supporting hematopoiesis of BMSCcon and BMSCgag. The results show that when compared to BMSCcon, BMSCgag reduced their proliferative activity and underwent senescence. The ability of BMSCgag to support the expansion of committed hematopoietic progenitors from umbilical cord blood-derived CD34(+)cells may be impaired, while the expression of genes associated with maintaining and enhancing hematopoiesis appeared to be decreased in treated BMSCs compared to control BMSCs. In conclusion, senescence induced by p55-gag resulted in decreased hematopoietic support function of BMSCs through reducing a series of hematopoietic cytokine expression.
机译：人类免疫缺陷病毒-1（HIV-1）感染患者通常存在造血失效。作为骨髓（BM）中的重要造血支持细胞，BM间充质干细胞（BMSCs）可以受到BM内受感染细胞释放的HIV蛋白的影响。在这项研究中，我们测试了HIV蛋白P55-GAG是否可以诱导BMSC的衰老，并降低其在体外支持造血干细胞的膨胀能力。用P55-GAG（BMSCGAG）慢性处理BMSCs长达20天，并将其增殖活性和衰老机与非加入细胞（BMSCCON）进行比较。然后，通过测定BMSCs上生长的造血祖细胞的细胞增殖，菌落形成能力和原始造血群分析了BMSCCON和BMSCGAG的造血支持功能。此外，我们比较了用于支持BMSCCON和BMSCGAG的血缺陷的基因表达模式。结果表明，与BMSCCON相比，BMSCGAG减少了它们的增殖活性并接受了衰老。 BMSCGAG支持从脐带血液衍生的CD34（+）细胞扩增的能力可能受损，同时与对照BMSCs的处理BMSCs相关的基因的表达似乎在处理的BMSC中降低。总之，P55-GAG诱导的衰老导致BMSCS的造血支持功能降低，通过减少一系列造血细胞因子表达。

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