• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>BMC Neuroscience >Neuronal hypoxia in vitro : Investigation of therapeutic principles of HUCB-MNC and CD133 + stem cells
【24h】

Neuronal hypoxia in vitro : Investigation of therapeutic principles of HUCB-MNC and CD133 + stem cells

机译：体外神经元缺氧：HUCB-MNC和CD133 +干细胞的治疗原理研究

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

摘要

Background The therapeutic capacity of human umbilical cord blood mononuclear cells (HUCB-MNC) and stem cells derived thereof is documented in animal models of focal cerebral ischemia, while mechanisms behind the reduction of lesion size and the observed improvement of behavioral skills still remain poorly understood. Methods A human in vitro model of neuronal hypoxia was used to address the impact of total HUCB-MNC (tMNC), a stem cell enriched fraction (CD133+, 97.38% CD133-positive cells) and a stem cell depleted fraction (CD133-, 0.06% CD133-positive cells) of HUCB-MNC by either direct or indirect co-cultivation with post-hypoxic neuronal cells (differentiated SH-SY5Y). Over three days, development of apoptosis and necrosis of neuronal cells, chemotaxis of MNC and production of chemokines (CCL2, CCL3, CCL5, CXCL8, CXCL9) and growth factors (G-CSF, GM-CSF, VEGF, bFGF) were analyzed using fluorescence microscopy, FACS and cytometric bead array. Results tMNC, CD133+ and surprisingly CD133- reduced neuronal apoptosis in direct co-cultivations significantly to levels in the range of normoxic controls (7% ± 3%). Untreated post-hypoxic control cultures showed apoptosis rates of 85% ± 11%. tMNC actively migrated towards injured neuronal cells. Both co-cultivation types using tMNC or CD133- reduced apoptosis comparably. CD133- produced high concentrations of CCL3 and neuroprotective G-CSF within indirect co-cultures. Soluble factors produced by CD133+ cells were not detectable in direct co-cultures. Conclusion Our data show that heterogeneous tMNC and even CD133-depleted fractions have the capability not only to reduce apoptosis in neuronal cells but also to trigger the retaining of neuronal phenotypes.
机译：背景技术在局灶性脑缺血的动物模型中记录了人类脐带血单核细胞（HUCB-MNC）及其衍生的干细胞的治疗能力，但对病灶缩小和观察到的行为技能改善背后的机制仍知之甚少。方法采用体外神经元缺氧模型，探讨总HUCB-MNC（tMNC），干细胞富集部分（CD133 + ，97.38％CD133阳性细胞）和干细胞的影响。通过与缺氧后神经元细胞（分化的SH-SY5Y）直接或间接共培养HUCB-MNC的细胞耗竭部分（CD133 -，0.06％CD133阳性细胞）。在三天的时间里，使用以下方法分析了神经元细胞的凋亡和坏死的发展，MNC的趋化性和趋化因子（CCL2，CCL3，CCL5，CXCL8，CXCL9）和生长因子（G-CSF，GM-CSF，VEGF，bFGF）的产生荧光显微镜，流式细胞仪和流式细胞仪。结果tMNC，CD133 + 和令人惊讶的CD133 -可以将直接共培养中的神经元凋亡显着降低至正常氧控制范围内的水平（7％±3％）。未经处理的低氧后对照培养物显示出85％±11％的细胞凋亡率。 tMNC主动向受损的神经元细胞迁移。使用tMNC或CD133 -的两种共培养类型均能降低凋亡。 CD133 -在间接共培养物中产生高浓度的CCL3和神经保护性G-CSF。在直接共培养中无法检测到CD133 + 细胞产生的可溶性因子。结论我们的数据表明，异质性tMNC甚至CD133耗尽的级分不仅具有减少神经元细胞凋亡的能力，而且具有触发神经元表型保留的能力。

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