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Differential expression of LeY and fucosyltransferase IV correlates with the receptivity of RL95‐2 and HEC‐1A human uterine epithelial cells
Author(s) -
Liu Shuai,
Yang Xuesong,
Wang Jiao,
Wei Jianxin,
Zhang Dongmei,
Wang Xiaoqi,
Yan Qiu
Publication year - 2012
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20100644
Subject(s) - fucosyltransferase , fucosylation , biology , transfection , microbiology and biotechnology , cell culture , endometrium , endocrinology , biochemistry , gene , genetics , glycoprotein , glycan
Adhesion molecules expressed on the uterine endometrium are potential receptive markers in embryo implantation. RL95‐2 and HEC‐1A cell lines represent the high‐ and low‐receptive endometrial epithelium respectively. LeY (Lewis Y) is a difucosylated oligosaccharide highly expressed in the endometrium of some species during implantation. α1, 3 fucosylation of LeY is catalysed by FUT4 (fucosyltransferase IV), the key synthesis enzyme for LeY. We investigated whether the difference in receptivity between the 2 cell lines was related to different expressions of LeY and FUT4. RL95‐2 cells expressed a higher level of LeY and FUT4 than HEC‐1A cells, as shown by immunofluorescent staining, RT—PCR (reverse transcription—PCR) or Western blotting. FUT4‐siRNA (small interfering RNA) transfection down‐regulated FUT4 and LeY in RL95‐2 cells, and inhibited the adhesion of the embryonic cells (JAR) to RL95‐2 cell monolayer. FUT4‐cDNA, however, increased the expression of FUT4 and LeY in HEC‐1A cells, and increased the adhesion of embryonic cells to HEC‐1A cell monolayer. Alterations of LeY level by up‐ or down‐regulation of FUT4 also mediated EGFR (epidermal growth factor receptor)/MAPK (mitogen‐activated protein kinase) signalling pathway. To conclude, the expression of LeY and FUT4 correlates with endometrial receptivity, making them potential new markers for the evaluation of endometrial receptivity.