Upregulation of GPR133 expression impaired the phagocytosis of macrophages in recurrent spontaneous miscarriage

ABSTRACTDecidual macrophages are the second-largest immune cell group at the maternal-foetal interface. They participate in apoptotic cell removal, and protect the foetus from microorganisms or pathogens. Dysfunction of decidual macrophages gives rise to pregnancy complications such as preeclampsia...

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Main Authors: Jia-Xue Sun, Yongli Yao, Wen-Xuan Li, Xin Su, Haoyu Yang, Zhouping Lu, Chenfei Liu, Xiang-Hong Xu, Liping Jin
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Epigenetics
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/15592294.2024.2337087
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author Jia-Xue Sun
Yongli Yao
Wen-Xuan Li
Xin Su
Haoyu Yang
Zhouping Lu
Chenfei Liu
Xiang-Hong Xu
Liping Jin
author_facet Jia-Xue Sun
Yongli Yao
Wen-Xuan Li
Xin Su
Haoyu Yang
Zhouping Lu
Chenfei Liu
Xiang-Hong Xu
Liping Jin
author_sort Jia-Xue Sun
collection DOAJ
description ABSTRACTDecidual macrophages are the second-largest immune cell group at the maternal-foetal interface. They participate in apoptotic cell removal, and protect the foetus from microorganisms or pathogens. Dysfunction of decidual macrophages gives rise to pregnancy complications such as preeclampsia and recurrent spontaneous miscarriage (RSM). However, the mechanisms by which decidual macrophages are involved in the occurrence of adverse pregnancy outcomes have not been elucidated. Here we integrated DNA methylation and gene expression data from decidua macrophages to identify potential risk factors related to RSM. GPR133 was significantly hypomethylated and upregulated in decidual macrophages from RSM patients. Further demethylation analysis demonstrated that GPR133 expression in decidual macrophages was significantly increased by 5-Aza-dC treatment. In addition, the influence of GPR133 on the phagocytic ability of macrophages was explored. Phagocytosis was impaired in the decidual macrophages of RSM patients with increased GPR133 expression. Increased GPR133 expression induced by demethylation treatment in the decidual macrophages of healthy control patients led to a significant decrease in phagocytic function. Importantly, knockdown of GPR133 resulted in a significant improvement in the phagocytic function of THP-1 macrophages. In conclusion, the existing studies have shown the influence of GPR133 on the phagocytic function of decidual macrophages and pregnancy outcomes, providing new data and ideas for future research on the role of decidual macrophages in RSM.
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spelling doaj.art-51dec0c1a3284d6da1859cdcec56f8112024-04-02T20:29:30ZengTaylor & Francis GroupEpigenetics1559-22941559-23082024-12-0119110.1080/15592294.2024.2337087Upregulation of GPR133 expression impaired the phagocytosis of macrophages in recurrent spontaneous miscarriageJia-Xue Sun0Yongli Yao1Wen-Xuan Li2Xin Su3Haoyu Yang4Zhouping Lu5Chenfei Liu6Xiang-Hong Xu7Liping Jin8Department of Biobank, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, P.R, ChinaDepartment of Biobank, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, P.R, ChinaDepartment of Biobank, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, P.R, ChinaDepartment of Biobank, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, P.R, ChinaDepartment of Biobank, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, P.R, ChinaDepartment of Biobank, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, P.R, ChinaDepartment of Biobank, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, P.R, ChinaDepartment of Biobank, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, P.R, ChinaDepartment of Biobank, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, P.R, ChinaABSTRACTDecidual macrophages are the second-largest immune cell group at the maternal-foetal interface. They participate in apoptotic cell removal, and protect the foetus from microorganisms or pathogens. Dysfunction of decidual macrophages gives rise to pregnancy complications such as preeclampsia and recurrent spontaneous miscarriage (RSM). However, the mechanisms by which decidual macrophages are involved in the occurrence of adverse pregnancy outcomes have not been elucidated. Here we integrated DNA methylation and gene expression data from decidua macrophages to identify potential risk factors related to RSM. GPR133 was significantly hypomethylated and upregulated in decidual macrophages from RSM patients. Further demethylation analysis demonstrated that GPR133 expression in decidual macrophages was significantly increased by 5-Aza-dC treatment. In addition, the influence of GPR133 on the phagocytic ability of macrophages was explored. Phagocytosis was impaired in the decidual macrophages of RSM patients with increased GPR133 expression. Increased GPR133 expression induced by demethylation treatment in the decidual macrophages of healthy control patients led to a significant decrease in phagocytic function. Importantly, knockdown of GPR133 resulted in a significant improvement in the phagocytic function of THP-1 macrophages. In conclusion, the existing studies have shown the influence of GPR133 on the phagocytic function of decidual macrophages and pregnancy outcomes, providing new data and ideas for future research on the role of decidual macrophages in RSM.https://www.tandfonline.com/doi/10.1080/15592294.2024.2337087Recurrent spontaneous miscarriagedecidual macrophageGPR133methylationphagocytosis
spellingShingle Jia-Xue Sun
Yongli Yao
Wen-Xuan Li
Xin Su
Haoyu Yang
Zhouping Lu
Chenfei Liu
Xiang-Hong Xu
Liping Jin
Upregulation of GPR133 expression impaired the phagocytosis of macrophages in recurrent spontaneous miscarriage
Epigenetics
Recurrent spontaneous miscarriage
decidual macrophage
GPR133
methylation
phagocytosis
title Upregulation of GPR133 expression impaired the phagocytosis of macrophages in recurrent spontaneous miscarriage
title_full Upregulation of GPR133 expression impaired the phagocytosis of macrophages in recurrent spontaneous miscarriage
title_fullStr Upregulation of GPR133 expression impaired the phagocytosis of macrophages in recurrent spontaneous miscarriage
title_full_unstemmed Upregulation of GPR133 expression impaired the phagocytosis of macrophages in recurrent spontaneous miscarriage
title_short Upregulation of GPR133 expression impaired the phagocytosis of macrophages in recurrent spontaneous miscarriage
title_sort upregulation of gpr133 expression impaired the phagocytosis of macrophages in recurrent spontaneous miscarriage
topic Recurrent spontaneous miscarriage
decidual macrophage
GPR133
methylation
phagocytosis
url https://www.tandfonline.com/doi/10.1080/15592294.2024.2337087
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