Embryonic undifferentiated cells show scattering activity on a surface coated with immobilized E‐cadherin

Embryonic undifferentiated cells show scattering activity on a surface coated with immobilized E‐cadherin
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DOI:
10.1002/jcb.21406
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发表时间:
2008
影响因子:
4
通讯作者:
M. Nagaoka;H. Ise;I. Harada;U. Koshimizu;A. Maruyama;T. Akaike
M. Nagaoka;H. Ise;I. Harada;U. Koshimizu;A. Maruyama;T. Akaike
中科院分区:
生物学2区
文献类型:
--
作者:
M. Nagaoka;H. Ise;I. Harada;U. Koshimizu;A. Maruyama;T. Akaike

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细胞间黏附重排是胚胎发育和组织形成过程中的重要事件。本研究以E-钙粘蛋白/Ig G Fc融合蛋白为黏附基质,在细胞培养中研究了E-钙粘蛋白在发育过程中的调控作用。当F9胚胎癌细胞在明胶或纤维连接蛋白基质上培养时,通常会形成集落。然而,在E-钙粘蛋白/Ig G Fc融合蛋白基质上培养的F9细胞形成了分散的分布,具有不同的细胞骨架结构和富含E-钙粘素的突起,这些突起受rac1活性的调节。在P19胚胎癌细胞中也观察到同样的散射活性。相反,三种分化细胞,NMuMG乳腺细胞、MDCK肾上皮细胞和小鼠原代分离的肝细胞,没有在F9和P19细胞中观察到的散射活性。这些结果表明,E-钙粘素固定的表面上的迁移行为只在胚胎细胞中观察到,并且E-钙粘附素介导的细胞黏附的调节机制随分化状态的不同而不同。J.细胞。生物化学。103:296-310,2008。©2007 Wiley-Liss Inc.
Rearrangement of cell–cell adhesion is a critical event in embryonic development and tissue formation. We investigated the regulatory function of E‐cadherin, a key adhesion protein, in the developmental process by using E‐cadherin/IgG Fc fusion protein as an adhesion matrix in cell culture. F9 embryonal carcinoma cells usually form colonies when cultured on gelatin or fibronectin matrices. However, F9 cells cultured on the E‐cadherin/IgG Fc fusion protein matrix formed a scattered distribution, with a different cytoskeletal organization and E‐cadherin‐rich protrusions that were regulated by Rac1 activity. The same scattering activity was observed in P19 embryonal carcinoma cells. In contrast, three types of differentiated cells, NMuMG mammary gland cells, MDCK kidney epithelial cells, and mouse primary isolated hepatocytes, did not show the scattering activity observed in F9 and P19 cells. These results suggest that migratory behavior on an E‐cadherin‐immobilized surface is only observed in embryonic cells, and that the regulatory mechanisms underlying E‐cadherin‐mediated cell adhesion vary with the state of differentiation. J. Cell. Biochem. 103: 296–310, 2008. © 2007 Wiley‐Liss, Inc.