...
首页> 外文期刊>Journal of cellular biochemistry. >Regulation of Adipose Tissue Stem Cells Angiogenic Potential by Tumor Necrosis Factor-Alpha
【24h】

Regulation of Adipose Tissue Stem Cells Angiogenic Potential by Tumor Necrosis Factor-Alpha

机译:肿瘤坏死因子-α对脂肪组织干细胞血管生成潜能的调控

获取原文
获取原文并翻译 | 示例
           

摘要

Tissue regeneration requires coordinated "teamwork" of growth factors, proteases, progenitor and immune cells producing inflammatory cytokines. Mesenchymal stem cells (MSC) might play a pivotal role by substituting cells or by secretion of growth factors or cytokines, and attraction of progenitor and inflammatory cells, which participate in initial stages of tissue repair. Due to obvious impact of inflammation on regeneration it seems promising to explore whether inflammatory factors could influence proangiogenic abilities of MSC. In this study we investigated effects of TNF-alpha on activity of adipose-derived stem cells (ADSC). We found that treatment with TNF-alpha enhances ADSC proliferation, F-actin microfilament assembly, increases cell motility and migration through extracellular matrix. Exposure of ADSC to TNF-alpha led to increased mRNA expression of proangiogenic factors (FGF-2, VEGF, IL-8, and MCP-1), inflammatory cytokines (IL-1b, IL-6), proteases (MMPs, uPA) and adhesion molecule ICAM-1. At the protein level, VEGF, IL-8, MCP-1, and ICAM-1 production was also up-regulated. Pre-incubation of ADSC with TNF-a-enhanced adhesion of monocytes to ADSC but suppressed adherence of ADSC to endothelial cells (HUVEC). Stimulation with TNF-alpha triggers ROS generation and activates a number of key intracellular signaling mediators known to positively regulate angiogenesis (Akt, small GTPase Rac1, ERK1/2, and p38 MAP-kinases). Pre-treatment with TNF-alpha-enhanced ADSC ability to promote growth of microvessels in a fibrin gel assay and accelerate blood flow recovery, which was accompanied by increased arteriole density and reduction of necrosis in mouse hind limb ischemia model. These findings indicate that TNF-alpha plays a role in activation of ADSC angiogenic and regenerative potential. (C) 2015 Wiley Periodicals, Inc.
机译:组织再生需要生长因子,蛋白酶,祖细胞和产生炎性细胞因子的免疫细胞的协调“协作”。间充质干细胞(MSC)可能通过替代细胞或通过生长因子或细胞因子的分泌以及祖细胞和炎性细胞的吸引而发挥关键作用,后者参与了组织修复的初始阶段。由于炎症对再生有明显影响,因此探索炎症因素是否会影响MSC的促血管生成能力似乎很有希望。在这项研究中,我们研究了TNF-α对脂肪干细胞(ADSC)活性的影响。我们发现用TNF-α治疗可增强ADSC增殖,F-肌动蛋白微丝组装,增加细胞运动性并通过细胞外基质迁移。 ADSC暴露于TNF-α会导致促血管生成因子(FGF-2,VEGF,IL-8和MCP-1),炎性细胞因子(IL-1b,IL-6),蛋白酶(MMP,uPA)的mRNA表达增加。和粘附分子ICAM-1。在蛋白质水平上,VEGF,IL-8,MCP-1和ICAM-1的产生也被上调。用TNF-a增强单核细胞与ADSC的粘附力预培养ADSC,但抑制ADSC与内皮细胞(HUVEC)的粘附力。 TNF-α刺激可触发ROS的产生,并激活许多关键的细胞内信号传导介质,这些介质可正向调节血管生成(Akt,小GTPase Rac1,ERK1 / 2和p38 MAP激酶)。 TNF-α增强的ADSC预处理能够在纤维蛋白凝胶测定中促进微血管生长并加速血流恢复,并伴有小鼠后肢缺血模型中的小动脉密度增加和坏死减少。这些发现表明,TNF-α在ADSC血管生成和再生潜能的激活中起作用。 (C)2015威利期刊公司

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