EphrinA1 stimulates cell attachment and inhibits cell aggregation through the EphA receptor pathway in human endometrial carcinoma-derived Ishikawa cells
EphrinA1 stimulates cell attachment and inhibits cell aggregation through the EphA receptor pathway in human endometrial carcinoma-derived Ishikawa cells
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DOI：
10.1093/humrep/der034
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发表时间：
2011-05-01
影响因子：
6.1
通讯作者：
Konishi, Ikuo
中科院分区：
文献类型：
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作者：
Fujii, Haruko;Fujiwara, Hiroshi;Konishi, Ikuo
背景技术背景：最近，Eph-ephrinA系统被提出有助于母体子宫内膜上皮和胚胎滋养外胚层之间的初始相互作用。由于Eph-ephrin相互作用可以诱导粘附力和/或排斥力进入细胞，我们研究了该系统在子宫内膜上皮细胞功能变化中的可能作用，使用子宫内膜癌衍生的石川cells.METHODS：EphA 1，A2和A4在石川细胞上的表达通过RT-PCR和Western印迹分析。结果：EphA 1、A2和A4在石川细胞上均有表达。重组ephrinA 1结合到石川细胞的表面并诱导EphA 2和A4的磷酸化。在牛血清白蛋白封闭的硝化纤维素包被的培养皿中，石川细胞保持漂浮并彼此聚集。在这些条件下，固定ephrinA 1促进石川细胞附着与增加的酪氨酸磷酸化的粘着斑激酶。此外，固定化ephrinA 1可逆地抑制石川细胞聚集。基因减少EphA 1，A2和A4的siRNA减弱了ephrinA 1对细胞聚集的抑制作用，证实ephrinA 1影响石川细胞功能通过Eph-ephrinA interaction.CONCLUSIONS：这项研究表明，Eph-ephrinA系统可以促进细胞附着沿着石川细胞的细胞间解离。这些结果表明，该系统可以诱导子宫内膜上皮细胞的功能变化。
BACKGROUND: Recently, the Eph-ephrinA system was proposed to contribute to the initial interaction between the maternal endometrial epithelium and embryonic trophectoderm. Since the Eph-ephrin interaction can induce adhesive and/or repulsive forces into the cells, we examined the possible role of this system in functional changes in endometrial epithelial cells using endometrial carcinoma-derived Ishikawa cells.METHODS: The expressions of EphA1, A2 and A4 on Ishikawa cells were examined by RT-PCR and western blotting analyses. The effects of recombinant ephrinA1 on Ishikawa cells were also examined by western blot analysis and cell attachment and aggregation assays.RESULTS: EphA1, A2 and A4 were expressed on Ishikawa cells. Recombinant ephrinA1 bound to the surfaces of Ishikawa cells and induced phosphorylation of EphA2 and A4. In bovine serum albumin-blocked nitrocellulose-coated dishes, Ishikawa cells remained floating and aggregated with each other. Under these conditions, immobilized ephrinA1 promoted Ishikawa cell attachment with increased tyrosine phosphorylation in focal adhesion kinase. In addition, immobilized ephrinA1 reversibly inhibited Ishikawa cell aggregation. Gene-reduction of EphA1, A2 and A4 by siRNAs attenuated the inhibitory effects of ephrinA1 on cell aggregation, confirming that ephrinA1 affects Ishikawa cell functions through Eph-ephrinA interaction.CONCLUSIONS: This study demonstrated that the Eph-ephrinA system can promote cell attachment along with intercellular dissociation in Ishikawa cells. These findings suggest that this system can induce functional changes in endometrial epithelial cells.