期刊文献+

SDF-1/CXCR4轴在缺氧缺血性脑损伤中的研究进展 被引量:10

Research progress in effects of SDF-1/CXCR4 axis on hypoxia-ischemia brain injury
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摘要 干细胞在许多组织器官显示巨大的细胞分化潜能,其治疗缺血缺氧性疾病成为当前研究的热点。已知局部缺血可诱导干细胞的动员,并能感受组织损伤而定向迁移到损伤区并进行分化。具有趋化因子受体4(CXC chemokine receptor 4,CXCR4)的干细胞迁移到高表达间质细胞来源的因子-1(stromal cell-derived factor-1,SDF-1)的组织区域,这种细胞的迁移运动能被CXCR4拈抗剂所阻断或通过CXCR4的过表达增强迁移的运动。SDF-1-CXCR4轴是体内各种类型的干细胞迁移及细胞在骨髓的滞留和归巢中的重要调节物质。本文就缺氧缺血性脑损伤的骨髓间质干细胞(bone marrow stromal cell,BMSC)治疗,SDF- 1-CXCR4轴在MSCs动员和损伤、修复中的作用作一综述。 Stem cells have exhibited great differentiation potentiality, which can be used in therapy for ischemiahypoxia diseases. Ischemia is known to induce mobilization of stem cells. The tissue injury is 'sensed' by the stem cells and they migrate to the site of damage and undergo differentiation. The SDF-1/CXCR4 axis is mediator for the migration of many types of stem cells and stagnation and homing of bone marrow cells. CXCR4 stem cells migrate to the sites highly expressing SDF-1.The ceils trafficking can be blocked by CXCR4 (CXC chemokine receptor 4) antagonist or enhanced by overexpression of CXCR4. The aim of this review is to summarize recent studies into the role of SDF-1/CXCR4 axis in migration and tissue recovery of bone marrow stromal cells and the BMSCs based therapy for hypoxia-ischemia brain damage.
出处 《生命科学》 CSCD 2008年第3期463-466,共4页 Chinese Bulletin of Life Sciences
基金 广东省科技计划项目(2005B50301012)
关键词 基质细胞衍生因子-1 迁移 干细胞 缺血缺氧 stromal cell-derived factor-l migrate stem cell hypoxia-ischemia brain injury
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参考文献29

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同被引文献203

  • 1刘菲,柳忠兰,刘淑杰.吸烟大鼠脑血管内皮细胞基质金属蛋白酶9的表达[J].中国动脉硬化杂志,2005,13(5):583-585. 被引量:2
  • 2戴永援,陈宝安.SDF-1/CXCR4与血液系统恶性肿瘤的关系研究进展[J].中国实验血液学杂志,2006,14(5):1056-1060. 被引量:2
  • 3王心蕊,何旭,王医术,李玉林.低氧促进人骨髓间充质干细胞迁移的实验研究[J].中国免疫学杂志,2006,22(12):1100-1102. 被引量:5
  • 4何觅春,李静,赵春华.低氧对间充质干细胞的影响[J].中国实验血液学杂志,2007,15(2):433-436. 被引量:11
  • 5中华人民共和国科学技术部.关于善待实验动物的指导性意见.2006.09-30
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  • 10Grayson WL,Zhao F, Izadpanah R,et al. Effects of hypoxia on human mesenchymal stem cell expansion and plasticity in 3D constructs. J Cell Physiol.2006;207(2):331-339.

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