Vascular endothelial growth factors A and C are induced in the SVZ following neonatal hypoxia-ischemia and exert different effects on neonatal glial progenitors.
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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新生儿缺氧 - 缺血性血症后，SVZ诱导了血管内皮生长因子A和C，对新生儿神经胶质祖细胞产生不同的影响。
DOI：
10.1007/s12975-012-0213-6
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发表时间：
2013-04
影响因子：
6.9
通讯作者：
Levison, Steven W.
中科院分区：
文献类型：
--
作者：
Bain, Jennifer M.;Moore, Lisamarie;Ren, Zhihua;Simonishvili, Sophia;Levison, Steven W.
关键词：
新生儿缺氧缺血 (H-I) 的发作与儿童脑瘫和多种其他神经功能缺损密切相关。修复受损器官所需的两个关键过程是增加能够再生受损细胞的前体细胞的数量，并将其分化为需要替换的细胞类型。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-I 损伤后组织修复的关键介质。本研究的目的是检验以下假设：某些 VEGF 同工型在新生儿 H-I 恢复期间增加，并且它们会对室下区 (SVZ) 祖细胞的增殖和分化产生不同的影响。在 H-I 的急性恢复期，SVZ 中短暂诱导 VEGF-A 和 VEGF-C，这与 SVZ 血管直径的增加相关。这些生长因子由神经胶质祖细胞、星形胶质细胞以及较小程度的小胶质细胞产生。 VEGF-A 促进 SVZ 神经胶质祖细胞产生星形胶质细胞，而 VEGF-C 刺激早期和晚期少突胶质细胞祖细胞的增殖，通过阻断 VEGFR-3 可以消除这种增殖。总而言之，这些结果为协调 SVZ 祖细胞对新生儿 H-I 反应的信号提供了新的见解。我们的研究进一步表明，延长 VEGF-C 产生的疗法和/或刺激 VEGFR-3 的激动剂将促进少突胶质祖细胞发育，从而增强围产期脑损伤后的髓鞘形成。
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.
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影响因子：
23.9
作者：
Shen Q;Wang Y;Kokovay E;Lin G;Chuang SM;Goderie SK;Roysam B;Temple S
通讯作者：
Temple S
影响因子：
5.3
作者：
Mani, N;Khaibullina, A;Rosenstein, JM
通讯作者：
Rosenstein, JM
DOI：
10.1073/pnas.182296499
发表时间：
2002-09-03
影响因子：
11.1
作者：
Jin, KL;Zhu, YH;Greenberg, DA
通讯作者：
Greenberg, DA
影响因子：
2.9
作者：
Matarredona, ER;Murillo-Carretero, M;Estrada, C
通讯作者：
Estrada, C
影响因子：
4.6
作者：
Hashimoto, Takao;Zhang, Xiang-Mei;Yang, Xian-Jie
通讯作者：
Yang, Xian-Jie