Vascular endothelial growth factor (VEGF) regulates cranial neural crest migration in vivo.
Vascular endothelial growth factor (VEGF) regulates cranial neural crest migration in vivo.
复制标题
血管内皮生长因子（VEGF）调节体内颅神经rest迁移。
DOI：
10.1016/j.ydbio.2009.12.022
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发表时间：
2010-03-01
影响因子：
2.7
通讯作者：
Kulesa PM
中科院分区：
文献类型：
--
作者：
McLennan R;Teddy JM;Kasemeier-Kulesa JC;Romine MH;Kulesa PM
神经嵴是研究胚胎细胞迁移的一个极佳模型，因为可以利用先进的光学成像和分子干预在体内研究细胞行为。尚不清楚的是分子信号如何引导神经嵴细胞（NCC）穿过多种微环境并迁移至特定靶点。在此，我们检验了这样一个假设：颅神经嵴细胞的侵入，特别是菱脑节4（r4）迁移流进入鳃弓2（ba2），是由于通过神经纤毛蛋白 - 1 - 血管内皮生长因子（VEGF）相互作用产生的化学吸引。我们发现外胚层中VEGF的时空表达模式与NCC迁移前沿相关。对r4迁移流的逆转录聚合酶链反应（RT - PCR）分析表明，ba2组织表达VEGF，r4神经嵴细胞表达VEGF受体2。当将可溶性VEGF受体1（sVEGFR1）注射到r4迁移前沿的远端以结合内源性VEGF时，神经嵴细胞无法完全侵入ba2。延时成像显示，在体外颅神经嵴细胞被ba2组织或VEGF来源所吸引。将浸泡有VEGF的珠子或表达VEGF的细胞放置在r4迁移流附近，会导致神经嵴细胞偏离常规路径并朝着异位的VEGF来源移动。我们的研究结果表明了一种模型，即神经嵴细胞进入和侵入ba2依赖于通过神经纤毛蛋白 - 1 - VEGF相互作用的化学吸引信号。
The neural crest is an excellent model to study embryonic cell migration, since cell behaviors can be studied in vivo with advanced optical imaging and molecular intervention. What is unclear is how molecular signals direct neural crest cell (NCC) migration through multiple microenvironments and into specific targets. Here, we tested the hypothesis that the invasion of cranial NCCs, specifically the rhombomere 4 (r4) migratory stream into branchial arch 2 (ba2), is due to chemoattraction through neuropilin-1-vascular endothelial growth factor (VEGF) interactions. We found that the spatio-temporal expression pattern of VEGF in the ectoderm correlated with the NCC migratory front. RT-PCR analysis of the r4 migratory stream showed that ba2 tissue expressed VEGF and r4 NCCs expressed VEGF receptor 2. When soluble VEGF receptor 1 (sVEGFR1) was injected distal to the r4 migratory front, to bind up endogenous VEGF, NCCs failed to completely invade ba2. Time-lapse imaging revealed that cranial NCCs were attracted to ba2 tissue or VEGF sources in vitro. VEGF-soaked beads or VEGF-expressing cells placed adjacent to the r4 migratory stream caused NCCs to divert from stereotypical pathways and move towards an ectopic VEGF source. Our results suggest a model in which NCC entry and invasion of ba2 is dependent on chemoattractive signaling through neuropilin-1-VEGF interactions.
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