Granulocyte colony-stimulating factor stimulates neurogenesis via vascular endothelial growth factor with STAT activation
Granulocyte colony-stimulating factor stimulates neurogenesis via vascular endothelial growth factor with STAT activation
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DOI：
10.1016/j.brainres.2005.12.037
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发表时间：
2006-02-16
期刊：
影响因子：
2.9
通讯作者：
Roh, JK
中科院分区：
文献类型：
--
作者：
Jung, KH;Chu, K;Roh, JK
成年人的大脑中有多能干细胞，它们位于支持自我更新的专门龛位中。粒细胞集落刺激因子（G-CSF）可诱导骨髓干细胞增殖并从其微环境中动员出来，并激活内皮细胞增殖，这可能有助于神经干细胞（NSCs）建立血管微环境。在这里，我们表明，G-CSF诱导受体介导的增殖和分化的神经前体细胞在人类神经干细胞培养和成年大鼠脑在体内。在培养的人神经干细胞中，G-CSF激活STAT 3和5，并增加VEGF及其受体VEGFR 2（Flk-1）的表达，VEGFR 2酪氨酸激酶抑制剂阻断GCSF刺激的神经发生。G-CSF还在体内激活成年大鼠脑中的内皮细胞增殖。我们的研究结果表明，G-CSF通过与VEGF和STAT激活的相互作用刺激神经发生。(c)2005 Elsevier B. V.保留所有权利。
The adult brain harbors multipotent stem cells, which reside in specialized niches that support self-renewal. Granulocyte colony- stimulating factor (G-CSF) induces bone marrow stem cells proliferation and mobilization from their niche, and activates endothelial cell proliferation, which might help to establish a vascular niche for neural stem cells (NSCs). Here, we show that G-CSF induced receptor- mediated proliferation and differentiation of neural precursors in human NSCs cultures and in adult rat brain in vivo. in human NSCs cultures, G-CSF activated STAT3 and 5, and increased VEGF and its receptor, VEGFR2 (Flk-1) expression, and VEGFR2 tyrosine kinase inhibitor blocked the neurogenesis stimulated by GCSF. G-CSF also activated endothelial cell proliferation in adult rat brain in vivo. Our results indicate that G-CSF stimulates neurogenesis through reciprocal interaction with VEGF and STAT activation. (c) 2005 Elsevier B.V. All rights reserved.