The neuroblast and angioblast chemotaxic factor SDF-1 (CXCL12) expression is briefly up regulated by reactive astrocytes in brain following neonatal hypoxic-ischemic injury.
The neuroblast and angioblast chemotaxic factor SDF-1 (CXCL12) expression is briefly up regulated by reactive astrocytes in brain following neonatal hypoxic-ischemic injury.
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新生儿缺氧 - 缺血性损伤后，大脑中的反应性星形胶质细胞简要调节神经细胞和血管细胞趋化因子SDF-1（CXCL12）表达。
DOI：
10.1186/1471-2202-6-63
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发表时间：
2005-10-31
期刊：
影响因子：
2.4
通讯作者：
Carroll, JE
中科院分区：
文献类型：
--
作者：
Miller, JT;Bartley, JH;Wimborne, HJC;Walker, AL;Hess, DC;Hill, WD;Carroll, JE
基质细胞衍生因子1(SDF-1或CXCL12)对表达CXCR4的骨髓来源细胞具有趋化作用。它在脑胚胎发育和对缺血损伤的反应中发挥作用，帮助引导神经母细胞迁移和血管生成。在实验性的成人中风模型中，SDF-1在损伤后30天的损伤区域的血管周围表达，表明它可能是组织修复策略的治疗靶点。我们假设SDF-1在新生儿脑缺氧缺血(HI)损伤后以类似的时间和空间模式表达。对25只7日龄C57BL/J小鼠进行了HI损伤。SDF-1的表达在伤后7d表达上调，但在以后的时间点不表达。SDF-1上调的主要部位是星形胶质细胞、其沿血管的足突和内皮细胞。SDF-1在HI损伤区血管中的定位表明，这些血管周围区域是细胞募集趋化信号的发源地，反应性星形胶质细胞是这一过程的主要中介。相关的内皮细胞可能是表达CXCR4受体的细胞进入损伤组织的血管附着和渗出的场所。在这里，我们显示，与成人相比，新生儿对骨髓来源细胞进行基于SDF-1的血管趋化募集的机会窗口要小得多。因此，在未经修饰的情况下，新生儿缺氧损伤后，内源性SDF-1介导的趋化和修复细胞的募集，包括外源性给药的干/祖细胞，只有一段很短的时间。
Stromal cell-derived factor 1 (SDF-1 or CXCL12) is chemotaxic for CXCR4 expressing bone marrow-derived cells. It functions in brain embryonic development and in response to ischemic injury in helping guide neuroblast migration and vasculogenesis. In experimental adult stroke models SDF-1 is expressed perivascularly in the injured region up to 30 days after the injury, suggesting it could be a therapeutic target for tissue repair strategies. We hypothesized that SDF-1 would be expressed in similar temporal and spatial patterns following hypoxic-ischemic (HI) injury in neonatal brain. Twenty-five 7-day-old C57BL/J mice underwent HI injury. SDF-1 expression was up regulated up to 7 days after the injury but not at the later time points. The chief sites of SDF-1 up regulation were astrocytes, their foot processes along blood vessels and endothelial cells. The localization of SDF-1 along blood vessels in the HI injury zone suggests that these perivascular areas are where chemotaxic signaling for cellular recruitment originates and that reactive astrocytes are major mediators of this process. The associated endothelium is likely to be the site for vascular attachment and diapedesis of CXCR4 receptor expressing cells to enter the injured tissue. Here we show that, relative to adults, neonates have a significantly smaller window of opportunity for SDF-1 based vascular chemotaxic recruitment of bone marrow-derived cells. Therefore, without modification, following neonatal HI injury there is only a narrow period of time for endogenous SDF-1 mediated chemotaxis and recruitment of reparative cells, including exogenously administered stem/progenitor cells.
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影响因子：
4.2
作者：
Peng, H;Huang, YL;Zheng, JL
通讯作者：
Zheng, JL
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