JAZF1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of G0S2
Abstract Decidualization of human endometrial stromal cells (hESCs) is essential for the maintenance of pregnancy, which depends on the fine-tuned regulation of hESCs survival, and its perturbation contributes to pregnancy loss. However, the underlying mechanisms responsible for functional deficits...
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2023-05-01
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| Series: | Communications Biology |
| Online Access: | https://doi.org/10.1038/s42003-023-04931-x |
| _version_ | 1797817859515088896 |
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| author | Yingyu Liang Siying Lai Lijun Huang Yulian Li Shanshan Zeng Shuang Zhang Jingsi Chen Wenbo Deng Yu Liu Jingying Liang Pei Xu Mingxing Liu Zhongtang Xiong Dunjin Chen Zhaowei Tu Lili Du |
| author_facet | Yingyu Liang Siying Lai Lijun Huang Yulian Li Shanshan Zeng Shuang Zhang Jingsi Chen Wenbo Deng Yu Liu Jingying Liang Pei Xu Mingxing Liu Zhongtang Xiong Dunjin Chen Zhaowei Tu Lili Du |
| author_sort | Yingyu Liang |
| collection | DOAJ |
| description | Abstract Decidualization of human endometrial stromal cells (hESCs) is essential for the maintenance of pregnancy, which depends on the fine-tuned regulation of hESCs survival, and its perturbation contributes to pregnancy loss. However, the underlying mechanisms responsible for functional deficits in decidua from recurrent spontaneous abortion (RSA) patients have not been elucidated. Here, we observed that JAZF1 was significantly downregulated in stromal cells from RSA decidua. JAZF1 depletion in hESCs resulted in defective decidualization and cell death through apoptosis. Further experiments uncovered G0S2 as a important driver of hESCs apoptosis and decidualization, whose transcription was repressed by JAZF1 via interaction with G0S2 activator Purβ. Moreover, the pattern of low JAZF1, high G0S2 and excessive apoptosis in decidua were consistently observed in RSA patients. Collectively, our findings demonstrate that JAZF1 governs hESCs survival and decidualization by repressing G0S2 transcription via restricting the activity of Purβ, and highlight the clinical implications of these mechanisms in the pathology of RSA. |
| first_indexed | 2024-03-13T08:59:40Z |
| format | Article |
| id | doaj.art-a7c83c468b324b1fa04d3fad773d5041 |
| institution | Directory Open Access Journal |
| issn | 2399-3642 |
| language | English |
| last_indexed | 2024-03-13T08:59:40Z |
| publishDate | 2023-05-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Communications Biology |
| spelling | doaj.art-a7c83c468b324b1fa04d3fad773d50412023-05-28T11:25:18ZengNature PortfolioCommunications Biology2399-36422023-05-016111710.1038/s42003-023-04931-xJAZF1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of G0S2Yingyu Liang0Siying Lai1Lijun Huang2Yulian Li3Shanshan Zeng4Shuang Zhang5Jingsi Chen6Wenbo Deng7Yu Liu8Jingying Liang9Pei Xu10Mingxing Liu11Zhongtang Xiong12Dunjin Chen13Zhaowei Tu14Lili Du15Department of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Fujian Provincial Key Laboratory of Reproductive Health Research, The First Affiliated Hospital of Xiamen University, Xiamen UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Pathology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityDepartment of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, Guangdong Engineering and Technology Research Center of Maternal-Fetal Medicine, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, The Third Affiliated Hospital of Guangzhou Medical UniversityAbstract Decidualization of human endometrial stromal cells (hESCs) is essential for the maintenance of pregnancy, which depends on the fine-tuned regulation of hESCs survival, and its perturbation contributes to pregnancy loss. However, the underlying mechanisms responsible for functional deficits in decidua from recurrent spontaneous abortion (RSA) patients have not been elucidated. Here, we observed that JAZF1 was significantly downregulated in stromal cells from RSA decidua. JAZF1 depletion in hESCs resulted in defective decidualization and cell death through apoptosis. Further experiments uncovered G0S2 as a important driver of hESCs apoptosis and decidualization, whose transcription was repressed by JAZF1 via interaction with G0S2 activator Purβ. Moreover, the pattern of low JAZF1, high G0S2 and excessive apoptosis in decidua were consistently observed in RSA patients. Collectively, our findings demonstrate that JAZF1 governs hESCs survival and decidualization by repressing G0S2 transcription via restricting the activity of Purβ, and highlight the clinical implications of these mechanisms in the pathology of RSA.https://doi.org/10.1038/s42003-023-04931-x |
| spellingShingle | Yingyu Liang Siying Lai Lijun Huang Yulian Li Shanshan Zeng Shuang Zhang Jingsi Chen Wenbo Deng Yu Liu Jingying Liang Pei Xu Mingxing Liu Zhongtang Xiong Dunjin Chen Zhaowei Tu Lili Du JAZF1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of G0S2 Communications Biology |
| title | JAZF1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of G0S2 |
| title_full | JAZF1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of G0S2 |
| title_fullStr | JAZF1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of G0S2 |
| title_full_unstemmed | JAZF1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of G0S2 |
| title_short | JAZF1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of G0S2 |
| title_sort | jazf1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of g0s2 |
| url | https://doi.org/10.1038/s42003-023-04931-x |
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