Forstreuter Frauke, Lucius Ralph, Mentlein Rolf
Department of Anatomy, University of Kiel, Olshausenstrasse 40, D-24098 Kiel, Germany.
J Neuroimmunol. 2002 Nov;132(1-2):93-8. doi: 10.1016/s0165-5728(02)00315-6.
Vascular endothelial growth factor (VEGF) is an angiogenic peptide that is produced in the brain after ischemia, injury or in malignant gliomas. Since these pathological conditions are associated with the infiltration of microglial cells, we investigated the expression of VEGF receptors (VEGFR) and possible effects of VEGF on cultivated microglial cells. As shown by reverse transcription-polymerase chain reaction and immunocytochemistry, rat microglial cells as well as the murine cell line BV-2 express the VEGFR-1, but not VEGFR-2. Murine VEGF induced 3H-thymidine incorporation into DNA of murine and rat microglial cells as well as chemotaxis in Boyden chamber assays. However, VEGF did not alter the phosphorylation of mitogen-activated protein kinases and only slightly that of the kinase Akt. These results show that microglial cells are targets for VEGF which induces migration and proliferation of these immunocompetent cells in the brain.
血管内皮生长因子（VEGF）是一种血管生成肽，在脑缺血、损伤后或恶性胶质瘤中产生。由于这些病理状况与小胶质细胞的浸润有关，我们研究了VEGF受体（VEGFR）的表达以及VEGF对培养的小胶质细胞的可能影响。逆转录-聚合酶链反应和免疫细胞化学结果显示，大鼠小胶质细胞以及小鼠细胞系BV-2表达VEGFR-1，但不表达VEGFR-2。小鼠VEGF在博伊登室试验中诱导3H-胸腺嘧啶掺入小鼠和大鼠小胶质细胞的DNA以及趋化作用。然而，VEGF并未改变丝裂原活化蛋白激酶的磷酸化，对激酶Akt的磷酸化影响也很小。这些结果表明，小胶质细胞是VEGF的作用靶点，VEGF可诱导这些脑内免疫活性细胞的迁移和增殖。
