Role of focal adhesion formation in migration and morphogenesis of endothelial cells
Role of focal adhesion formation in migration and morphogenesis of endothelial cells
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DOI：
10.1016/j.cellsig.2004.03.010
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发表时间：
2004-11-01
影响因子：
4.8
通讯作者：
Kanetake, H
中科院分区：
文献类型：
--
作者：
Kanda, S;Miyata, Y;Kanetake, H
细胞运动和形态发生由应力纤维和粘着斑的形成和分解之间的平衡调节。为了了解血管生成中这些细胞反应的机制，我们研究了 FGF-2 诱导的小鼠脑毛细血管内皮细胞系 IBE 细胞的趋化性和毛细血管形态发生中 Rho 家族蛋白驱动的途径。接种到纤连蛋白包被表面的细胞向 FGF-2 迁移。显性失活 Rho A (DNRho) 或激酶死亡 p21 激活激酶 1 (KDPAK1) 的表达，或用 Y27632 治疗抑制趋化性，这与缺乏 FGF-2 诱导的粘着斑减少有关。在基质胶上，DNRho 和 Y27632 诱导了不依赖于 FGF-2 的毛细血管形态发生，尽管应力纤维形成丧失。 KDPAK1 细胞响应 FGF-2 形成应力纤维并表现出毛细血管形态发生。粘着斑的增加与毛细血管形态发生密切相关。我们的结果表明，粘着斑的形成或分解似乎决定了内皮细胞的运动或形态发生。 (C) 2004 Elsevier Inc. 保留所有权利。
Cell motility and morphogenesis are regulated by a balance between formation and disassembly of stress fibers and focal adhesions. To understand the mechanisms underlying these cellular responses in angiogenesis, we studied the Rho family protein-driven pathways in FGF-2-induced chemotaxis and capillary morphogenesis of murine brain capillary endothelial cell line, IBE cells. Cells seeded onto fibronectin-coated surface migrated toward FGF-2. Expression of dominant negative Rho A (DNRho) or kinase-dead p21-activated kinase 1 (KDPAK1), or treatment with Y27632 inhibited chemotaxis in association with the lack of FGF-2-induced decrease in focal adhesions. On Matrigel, DNRho and Y27632 induced FGF-2-independent capillary morphogenesis despite loss of stress fiber formation. KDPAK1 cells formed stress fibers and showed capillary morphogenesis in response to FGF-2. Increase in focal adhesions was closely associated with capillary morphogenesis. Our results suggest that formation or disassembly of focal adhesions seems to determine the motility or morphogenesis of endothelial cells. (C) 2004 Elsevier Inc. All rights reserved.