Glycomics reveal that ST6GAL1-mediated sialylation regulates uterine lumen closure during implantation.
Glycomics reveal that ST6GAL1-mediated sialylation regulates uterine lumen closure during implantation.
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糖组学揭示 ST6GAL1 介导的唾液酸化在着床过程中调节子宫腔关闭
DOI：
10.1111/cpr.13169
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发表时间：
2022-01
影响因子：
8.5
通讯作者：
Yu M
中科院分区：
文献类型：
--
作者：
Han K;Wang F;Yue Y;Tan X;Tian M;Miao Y;Zhao S;Dong W;Yu M
Implantation failure is a major cause of prenatal mortality. The uterine lumen closure contributes to embryo adhesion to the uterus, but its underlying mechanisms are largely unknown. Our previous study has reported that endometrial fold extension can lead to uterine lumen closure in pigs. The objective of this study was to reveal molecular mechanisms of the uterine lumen closure by characterizing the molecular basis of the endometrial fold extension during implantation in pigs. Uterine and endometrium tissues during implantation were collected in pigs. MALDI‐TOF MS was used to characterize the N‐glycomic profiles. Histochemistry, siRNA transfection, Western blotting, lectin immumoprecipitation, mass spectrometry and assays of wounding healing and cell aggregation were performed to investigate the molecular basis. We observed that uterine luminal epithelium (LE) migrated collectively during endometrial fold extension. For the first time, we identified a large number of N‐glycan compositions from endometrium during implantation using MALDI‐TOF MS. Notably, the α2,6‐linked sialic acid and ST6GAL1 were highly expressed in uterine LE when the endometrial folds extended greatly. Subsequently, the role of ST6GAL1‐mediated 2,6‐sialylation in collective epithelial migration was demonstrated. Finally, we found that ST6GAL1‐mediated α2,6‐sialylation of E‐cadherin may participate in collective migration of uterine LE. The study reveals a mechanism of uterine lumen closure by identifying that ST6GAL1‐mediated α2,6‐sialylation of cell adhesion molecules contributes to endometrial fold extension through regulating collective migration of uterine LE. Effect of α2,6‐sialylation mediated by ST6GAL1 on regulation of pig endometrial folds extending during implantation. The ST6GAL1 mediated α2,6‐sialylation of cell adhesion molecular, such as E‐cadherin, alters the stability of the cell‐cell adherens junction, participates in activation of Rac1/WAVE1 signal pathway to regulate the collective migration of uterine LE and leads to the extending of endometrial folds during implantation.
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影响因子：
16
作者：
Lebensohn AM;Kirschner MW
通讯作者：
Kirschner MW
影响因子：
9.2
作者：
Mehidi, Amine;Rossier, Olivier;Giannone, Gregory
通讯作者：
Giannone, Gregory
影响因子：
64.8
作者：
Barriga EH;Franze K;Charras G;Mayor R
通讯作者：
Mayor R
影响因子：
9
作者：
Blois SM;Verlohren S;Wu G;Clark G;Dell A;Haslam SM;Barrientos G
通讯作者：
Barrientos G
空间转录组和 miRNA 分析揭示了参与猪系膜偏向着床的基因
影响因子：
3.5
作者：
Huang, Ji;Yang, Yifen;Yu, Mei
通讯作者：
Yu, Mei