Galectin-4 expression is down-regulated in response to autophagy during differentiation of rat trophoblast cells.

Galectin-4 expression is down-regulated in response to autophagy during differentiation of rat trophoblast cells.
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DOI:
10.1038/srep32248
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发表时间:
2016-08-30
期刊:
影响因子:
4.6
通讯作者:
Shoji H
Shoji H
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Arikawa T;Liao S;Shimada H;Inoue T;Sakata-Haga H;Nakamura T;Hatta T;Shoji H

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Placental development and trophoblast invasion of the maternal endometrium establish the maternal-fetal interface, which is critical for the developing embryo and fetus. Herein we show that overexpression of Galectin-4 (Gal-4) during trophoblast differentiation inhibited the enlargement of Rcho-1 cells (a model for rat trophoblast differentiation) and promoted cell-cell adhesion, whereas trophoblast specific markers and MMP-9 activity were not affected. In the rat placenta, microtubule associated protein 1 light chain 3 alpha (LC3) protein, an autophagy marker, is highly expressed on the maternal side of the decidua where Gal-4 expression is weak. In vitro assays showed that the expression of trophoblast-specific differentiation markers was reduced by 3-Methyladenine (3-MA) and Bafilomycin A1, known as autophagy inhibitors, compared to control cells. Furthermore, Gal-4 expression in Rcho-1 cells, which is normally down-regulated during differentiation, was not attenuated in the presence of autophagy inhibitors, suggesting that autophagy is upstream of Gal-4 expression. We herein describe a possible mechanism by which autophagy regulates trophoblast differentiation via regulation of Gal-4 expression in order to establish the maternal-fetal interface.
Galectin-4 可作为肝细胞癌早期复发/转移的预后生物标志物。
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