Loss of CDYL Results in Suppression of CTNNB1 and Decreased Endometrial Receptivity

Impaired endometrial receptivity is one of the major causes of recurrent implantation failure (RIF), although the underlying molecular mechanism has not been fully elucidated. In the present study, we demonstrated that chromodomain Y like (CDYL) was highly expressed in the endometrium at mid-secreto...

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Main Authors: Xiaowei Zhou, Bufang Xu, Dan Zhang, Xiaoping Jiang, Hsun-Ming Chang, Peter C. K. Leung, Xiaoyu Xia, Aijun Zhang
Format: Article
Language:English
Published: Frontiers Media S.A. 2020-02-01
Series:Frontiers in Cell and Developmental Biology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fcell.2020.00105/full
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author Xiaowei Zhou
Bufang Xu
Dan Zhang
Xiaoping Jiang
Hsun-Ming Chang
Peter C. K. Leung
Xiaoyu Xia
Xiaoyu Xia
Aijun Zhang
Aijun Zhang
author_facet Xiaowei Zhou
Bufang Xu
Dan Zhang
Xiaoping Jiang
Hsun-Ming Chang
Peter C. K. Leung
Xiaoyu Xia
Xiaoyu Xia
Aijun Zhang
Aijun Zhang
author_sort Xiaowei Zhou
collection DOAJ
description Impaired endometrial receptivity is one of the major causes of recurrent implantation failure (RIF), although the underlying molecular mechanism has not been fully elucidated. In the present study, we demonstrated that chromodomain Y like (CDYL) was highly expressed in the endometrium at mid-secretory phase during the normal menstrual cycles. However, the expression of CDYL was downregulated in the endometrial tissues obtained from women with RIF, consistently with the protein level of LIF, which is a marker of endometrial receptivity. In CDYL-knockdown human endometrial Ishikawa cells, we identified 1738 differentially expressed genes (DEGs). Importantly, the catenin beta 1 (CTNNB1) expression was dramatically reduced responding to the CDYL inhibition, both in Ishikawa cells as well as the primary endometrial epithelial and stromal cells. In addition, the expression of CTNNB1was decreased in the endometrium from RIF patients as well. These results suggested that the expression of CTNNB1 was regulated by CDYL in endometrium. The cell migration was impaired by CDYL-knockdown in Ishikawa cells and primary endometrial stromal cells (ESCs), which could be rescued by CDYL or CTNNB1 overexpression. Collectively, our findings indicated that the decreased expression of CDYL may suppress endometrial cell migration capability by affecting CTNNB1 expression, which would contribute to poor endometrial receptivity in women with RIF.
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spelling doaj.art-63a0f39d23594e32b8d18737721941c42022-12-21T19:15:36ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2020-02-01810.3389/fcell.2020.00105510445Loss of CDYL Results in Suppression of CTNNB1 and Decreased Endometrial ReceptivityXiaowei Zhou0Bufang Xu1Dan Zhang2Xiaoping Jiang3Hsun-Ming Chang4Peter C. K. Leung5Xiaoyu Xia6Xiaoyu Xia7Aijun Zhang8Aijun Zhang9Department of Reproductive Medical Center, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Reproductive Medical Center, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Reproductive Medical Center, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Obstetrics and Gynecology, Chinese People’s Armed Police Force Shanghai Corps Hospital, Shanghai, ChinaDepartment of Obstetrics and Gynaecology, BC Children’s Hospital Research Institute, The University of British Columbia, Vancouver, BC, CanadaDepartment of Obstetrics and Gynaecology, BC Children’s Hospital Research Institute, The University of British Columbia, Vancouver, BC, CanadaDepartment of Histoembryology, Genetics and Developmental Biology, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaShanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Reproductive Medical Center, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaShanghai Key Laboratory of Reproductive Medicine, Shanghai Jiao Tong University, Shanghai, ChinaImpaired endometrial receptivity is one of the major causes of recurrent implantation failure (RIF), although the underlying molecular mechanism has not been fully elucidated. In the present study, we demonstrated that chromodomain Y like (CDYL) was highly expressed in the endometrium at mid-secretory phase during the normal menstrual cycles. However, the expression of CDYL was downregulated in the endometrial tissues obtained from women with RIF, consistently with the protein level of LIF, which is a marker of endometrial receptivity. In CDYL-knockdown human endometrial Ishikawa cells, we identified 1738 differentially expressed genes (DEGs). Importantly, the catenin beta 1 (CTNNB1) expression was dramatically reduced responding to the CDYL inhibition, both in Ishikawa cells as well as the primary endometrial epithelial and stromal cells. In addition, the expression of CTNNB1was decreased in the endometrium from RIF patients as well. These results suggested that the expression of CTNNB1 was regulated by CDYL in endometrium. The cell migration was impaired by CDYL-knockdown in Ishikawa cells and primary endometrial stromal cells (ESCs), which could be rescued by CDYL or CTNNB1 overexpression. Collectively, our findings indicated that the decreased expression of CDYL may suppress endometrial cell migration capability by affecting CTNNB1 expression, which would contribute to poor endometrial receptivity in women with RIF.https://www.frontiersin.org/article/10.3389/fcell.2020.00105/fullrecurrent implantation failurechromodomain Y likecatenin beta 1migrationendometrial receptivity
spellingShingle Xiaowei Zhou
Bufang Xu
Dan Zhang
Xiaoping Jiang
Hsun-Ming Chang
Peter C. K. Leung
Xiaoyu Xia
Xiaoyu Xia
Aijun Zhang
Aijun Zhang
Loss of CDYL Results in Suppression of CTNNB1 and Decreased Endometrial Receptivity
Frontiers in Cell and Developmental Biology
recurrent implantation failure
chromodomain Y like
catenin beta 1
migration
endometrial receptivity
title Loss of CDYL Results in Suppression of CTNNB1 and Decreased Endometrial Receptivity
title_full Loss of CDYL Results in Suppression of CTNNB1 and Decreased Endometrial Receptivity
title_fullStr Loss of CDYL Results in Suppression of CTNNB1 and Decreased Endometrial Receptivity
title_full_unstemmed Loss of CDYL Results in Suppression of CTNNB1 and Decreased Endometrial Receptivity
title_short Loss of CDYL Results in Suppression of CTNNB1 and Decreased Endometrial Receptivity
title_sort loss of cdyl results in suppression of ctnnb1 and decreased endometrial receptivity
topic recurrent implantation failure
chromodomain Y like
catenin beta 1
migration
endometrial receptivity
url https://www.frontiersin.org/article/10.3389/fcell.2020.00105/full
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