Targeting CD301+ macrophages inhibits endometrial fibrosis and improves pregnancy outcome

Abstract Macrophages are a key and heterogeneous cell population involved in endometrial repair and regeneration during the menstrual cycle, but their role in the development of intrauterine adhesion (IUA) and sequential endometrial fibrosis remains unclear. Here, we reported that CD301+ macrophages...

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Main Authors: Haining Lv, Haixiang Sun, Limin Wang, Simin Yao, Dan Liu, Xiwen Zhang, Zhongrui Pei, Jianjun Zhou, Huiyan Wang, Jianwu Dai, Guijun Yan, Lijun Ding, Zhiyin Wang, Chenrui Cao, Guangfeng Zhao, Yali Hu
Format: Article
Language:English
Published: Springer Nature 2023-07-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.202317601
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author Haining Lv
Haixiang Sun
Limin Wang
Simin Yao
Dan Liu
Xiwen Zhang
Zhongrui Pei
Jianjun Zhou
Huiyan Wang
Jianwu Dai
Guijun Yan
Lijun Ding
Zhiyin Wang
Chenrui Cao
Guangfeng Zhao
Yali Hu
author_facet Haining Lv
Haixiang Sun
Limin Wang
Simin Yao
Dan Liu
Xiwen Zhang
Zhongrui Pei
Jianjun Zhou
Huiyan Wang
Jianwu Dai
Guijun Yan
Lijun Ding
Zhiyin Wang
Chenrui Cao
Guangfeng Zhao
Yali Hu
author_sort Haining Lv
collection DOAJ
description Abstract Macrophages are a key and heterogeneous cell population involved in endometrial repair and regeneration during the menstrual cycle, but their role in the development of intrauterine adhesion (IUA) and sequential endometrial fibrosis remains unclear. Here, we reported that CD301+ macrophages were significantly increased and showed their most active interaction with profibrotic cells in the endometria of IUA patients compared with the normal endometria by single‐cell RNA sequencing, bulk RNA sequencing, and experimental verification. Increasing CD301+ macrophages promoted the differentiation of endometrial stromal cells into myofibroblasts and resulted in extracellular matrix accumulation, which destroyed the physiological architecture of endometrial tissue, drove endometrial fibrosis, and ultimately led to female infertility or adverse pregnancy outcomes. Mechanistically, CD301+ macrophages secreted GAS6 to activate the AXL/NF‐κB pathway, upregulating the profibrotic protein synthesis. Targeted deletion of CD301+ macrophages or inhibition of AXL by Bemcentinib blunted the pathology and improved the outcomes of pregnancy in mice, supporting the therapeutic potential of targeting CD301+ macrophages for treating endometrial fibrosis.
format Article
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institution DOAJ
issn 1757-4676
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language English
publishDate 2023-07-01
publisher Springer Nature
record_format Article
series EMBO Molecular Medicine
spelling doaj-art-140882d6042c44ef84d10e0a062db7372025-08-20T03:05:53ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842023-07-0115911910.15252/emmm.202317601Targeting CD301+ macrophages inhibits endometrial fibrosis and improves pregnancy outcomeHaining Lv0Haixiang Sun1Limin Wang2Simin Yao3Dan Liu4Xiwen Zhang5Zhongrui Pei6Jianjun Zhou7Huiyan Wang8Jianwu Dai9Guijun Yan10Lijun Ding11Zhiyin Wang12Chenrui Cao13Guangfeng Zhao14Yali Hu15Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityCenter for Reproductive Medicine and Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityNanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese MedicineCenter for Reproductive Medicine and Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityInstitute of Genetics and Developmental Biology, Chinese Academy of SciencesCenter for Reproductive Medicine and Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityCenter for Reproductive Medicine and Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityDepartment of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing UniversityAbstract Macrophages are a key and heterogeneous cell population involved in endometrial repair and regeneration during the menstrual cycle, but their role in the development of intrauterine adhesion (IUA) and sequential endometrial fibrosis remains unclear. Here, we reported that CD301+ macrophages were significantly increased and showed their most active interaction with profibrotic cells in the endometria of IUA patients compared with the normal endometria by single‐cell RNA sequencing, bulk RNA sequencing, and experimental verification. Increasing CD301+ macrophages promoted the differentiation of endometrial stromal cells into myofibroblasts and resulted in extracellular matrix accumulation, which destroyed the physiological architecture of endometrial tissue, drove endometrial fibrosis, and ultimately led to female infertility or adverse pregnancy outcomes. Mechanistically, CD301+ macrophages secreted GAS6 to activate the AXL/NF‐κB pathway, upregulating the profibrotic protein synthesis. Targeted deletion of CD301+ macrophages or inhibition of AXL by Bemcentinib blunted the pathology and improved the outcomes of pregnancy in mice, supporting the therapeutic potential of targeting CD301+ macrophages for treating endometrial fibrosis.https://doi.org/10.15252/emmm.202317601CD301+ macrophagesendometrial fibrosisintrauterine adhesionpregnancy outcome
spellingShingle Haining Lv
Haixiang Sun
Limin Wang
Simin Yao
Dan Liu
Xiwen Zhang
Zhongrui Pei
Jianjun Zhou
Huiyan Wang
Jianwu Dai
Guijun Yan
Lijun Ding
Zhiyin Wang
Chenrui Cao
Guangfeng Zhao
Yali Hu
Targeting CD301+ macrophages inhibits endometrial fibrosis and improves pregnancy outcome
EMBO Molecular Medicine
CD301+ macrophages
endometrial fibrosis
intrauterine adhesion
pregnancy outcome
title Targeting CD301+ macrophages inhibits endometrial fibrosis and improves pregnancy outcome
title_full Targeting CD301+ macrophages inhibits endometrial fibrosis and improves pregnancy outcome
title_fullStr Targeting CD301+ macrophages inhibits endometrial fibrosis and improves pregnancy outcome
title_full_unstemmed Targeting CD301+ macrophages inhibits endometrial fibrosis and improves pregnancy outcome
title_short Targeting CD301+ macrophages inhibits endometrial fibrosis and improves pregnancy outcome
title_sort targeting cd301 macrophages inhibits endometrial fibrosis and improves pregnancy outcome
topic CD301+ macrophages
endometrial fibrosis
intrauterine adhesion
pregnancy outcome
url https://doi.org/10.15252/emmm.202317601
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