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首页> 美国卫生研究院文献>other >Vascular endothelial growth factors A and C are induced in the SVZ following neonatal hypoxia-ischemia and exert different effects on neonatal glial progenitors
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Vascular endothelial growth factors A and C are induced in the SVZ following neonatal hypoxia-ischemia and exert different effects on neonatal glial progenitors

机译：新生鼠缺氧缺血后在SVZ中诱导血管内皮生长因子A和C对新生胶质祖细胞产生不同的作用

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Episodes of neonatal hypoxia-ischemia (H-I) are strongly associated with cerebral palsy and a wide spectrum of other neurological deficits in children. Two key processes required to repair damaged organs are to amplify the number of precursors capable of regenerating damaged cells and to direct their differentiation towards the cell types that need to be replaced. Since hypoxia induces vascular endothelial growth factor (VEGF) production, it is logical to predict that VEGFs are key mediators of tissue repair after H-I injury. The goal of this study was to test the hypothesis that certain VEGF isoforms increase during recovery from neonatal H-I and that they would differentially affect the proliferation and differentiation of subventricular zone (SVZ) progenitors. During the acute recovery period from H-I both VEGF-A and VEGF-C were transiently induced in the SVZ, which correlated with an increase in SVZ blood vessel diameter. These growth factors were produced by glial progenitors, astrocytes and to a lesser extent, microglia. VEGF-A promoted the production of astrocytes from SVZ glial progenitors while VEGF-C stimulated the proliferation of both early and late oligodendrocyte progenitors, which was abolished by blocking the VEGFR-3. Altogether, these results provide new insights into the signals that coordinate the reactive responses of the progenitors in the SVZ to neonatal H-I. Our studies further suggest that therapeutics that extend VEGF-C production and/or agonists that stimulate the VEGFR-3 will promote oligodendrocyte progenitor cell development to enhance myelination after perinatal brain injury.
机译：新生儿缺氧缺血（H-I）发作与儿童的脑瘫和其他广泛的神经系统缺陷密切相关。修复受损器官所需的两个关键过程是放大能够再生受损细胞的前体数量，并将其分化方向引导至需要更换的细胞类型。由于缺氧会诱导血管内皮生长因子（VEGF）的产生，因此可以合理地预测VEGF是H-1损伤后组织修复的关键介质。这项研究的目的是检验以下假设：从新生儿H-1恢复期间，某些VEGF亚型会增加，并且它们会差异地影响脑室下（SVZ）祖细胞的增殖和分化。在从H-1的急性恢复期中，在SVZ中瞬时诱导了VEGF-A和VEGF-C，这与SVZ血管直径的增加相关。这些生长因子是由神经胶质祖细胞，星形胶质细胞和小胶质细胞产生的。 VEGF-A促进了SVZ胶质祖细胞产生星形胶质细胞，而VEGF-C刺激了早期和晚期少突胶质细胞祖细胞的增殖，这通过阻断VEGFR-3而被消除。总之，这些结果为协调SVZ中祖细胞对新生儿H-1的反应提供了新的见解。我们的研究进一步表明，延长VE​​GF-C产生和/或刺激VEGFR-3的激动剂的疗法将促进少突胶质细胞祖细胞的发育，从而增强围产期脑损伤后的髓鞘形成。

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