TBC1D20 is Essential for Postnatal Uterine Development and Endometrial Decidualization in Mice
Background: TBC1 domain family member 20 (TBC1D20) is important in male reproductive, eye lens function and neural system development. However, the role of TBC1D20 on reproduction in female mice remain unclear. Methods: As a prospective laboratory-based study, a mouse model with spontaneous function...
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| Format: | Article |
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IMR Press
2024-06-01
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| Series: | Clinical and Experimental Obstetrics & Gynecology |
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| Online Access: | https://www.imrpress.com/journal/CEOG/51/6/10.31083/j.ceog5106146 |
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| author | Wenpeng Min Xi Li Jing Zhou Wei Yuan Qing Yang Xinmei Ji Bing Liu Liqiong Luo Yuxia He Lina Cui Wen-Lin Chang |
| author_facet | Wenpeng Min Xi Li Jing Zhou Wei Yuan Qing Yang Xinmei Ji Bing Liu Liqiong Luo Yuxia He Lina Cui Wen-Lin Chang |
| author_sort | Wenpeng Min |
| collection | DOAJ |
| description | Background: TBC1 domain family member 20 (TBC1D20) is important in male reproductive, eye lens function and neural system development. However, the role of TBC1D20 on reproduction in female mice remain unclear. Methods: As a prospective laboratory-based study, a mouse model with spontaneous functional mutations of Tbc1d20 (Tbc1d20-/-) was employed to investigate the effect of Tbc1d20 on the fertility of female. Then the role of Tbc1d20 on postnatal female reproductive tract development and gonadal function was measured by immunohistochemistry assay and radioimmunoassay. A bilateral ovarian removal model and an artificial induced decidualization model were employed to reveal the function of Tbc1d20 on endometrial decidualization in vivo. Primary uterine stromal cells were isolated to evaluate the effect of Tbc1d20 on uterine stromal cell proliferation and the ability of decidualization in vitro. Results: Female Tbc1d20-/- mice were infertile. Functional mutations of Tbc1d20 exerted no obvious changes on the function of ovary, structure of fallopian tubes, and ability of early embryo implantation. However, Tbc1d20-/- mice presented marked reduction on the uterine size and weight at two-month-old, accompanied limitations on the myometrial thickness, the number of endometrial glands, and the density of blood vessels. Tbc1d20-/- mice exhibited an impaired uterine decidualization phenotype in vivo. In addition, in vitro primary cell model indicated that the proliferation and differentiation of uterine stromal cells were retarded while Tbc1d20 loss of function. Mechanically, TBC1D20 deficiency triggered endoplasmic reticulum stress in proliferating and differentiating uterine stromal cells. Conclusions: The findings from this study indicated that TBC1D20 is necessary for normal postnatal uterine development and endometrial decidualization in mice. |
| format | Article |
| id | doaj-art-4cf791f112a34782845fb5a6e40c3e43 |
| institution | OA Journals |
| issn | 0390-6663 |
| language | English |
| publishDate | 2024-06-01 |
| publisher | IMR Press |
| record_format | Article |
| series | Clinical and Experimental Obstetrics & Gynecology |
| spelling | doaj-art-4cf791f112a34782845fb5a6e40c3e432025-08-20T01:56:45ZengIMR PressClinical and Experimental Obstetrics & Gynecology0390-66632024-06-0151614610.31083/j.ceog5106146S0390-6663(24)02365-0TBC1D20 is Essential for Postnatal Uterine Development and Endometrial Decidualization in MiceWenpeng Min0Xi Li1Jing Zhou2Wei Yuan3Qing Yang4Xinmei Ji5Bing Liu6Liqiong Luo7Yuxia He8Lina Cui9Wen-Lin Chang10College of Veterinary Medicine, Hunan Agricultural University, 410128 Changsha, Hunan, ChinaDepartment of Orthopaedics and Traumatology, The People's Hospital of Longhua Shenzhen, 518109 Shenzhen, Guangdong, ChinaDepartment of Obstetrics, The People's Hospital of Longhua Shenzhen, 518109 Shenzhen, Guangdong, ChinaCollege of Veterinary Medicine, Hunan Agricultural University, 410128 Changsha, Hunan, ChinaCollege of Veterinary Medicine, Hunan Agricultural University, 410128 Changsha, Hunan, ChinaDepartment of Gynaecology, The People's Hospital of Longhua Shenzhen, 518109 Shenzhen, Guangdong, ChinaDepartment of Gynaecology, The People's Hospital of Longhua Shenzhen, 518109 Shenzhen, Guangdong, ChinaDepartment of Obstetrics, The People's Hospital of Longhua Shenzhen, 518109 Shenzhen, Guangdong, ChinaDepartment of Obstetrics and Gynaecology, Center for Reproductive Medicine, Key Laboratary for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital of Guangzhou Medical University, 510150 Guangzhou, Guangdong, ChinaGuangdong and Shenzhen Key Laboratory of Male Reproductive Medicine and Genetics, Peking University Shenzhen Hospital, Shenzhen Peking University-Hong Kong University of Science and Technology Medical Center, 518036 Shenzhen, Guangdong, ChinaDepartment of Obstetrics, The People's Hospital of Longhua Shenzhen, 518109 Shenzhen, Guangdong, ChinaBackground: TBC1 domain family member 20 (TBC1D20) is important in male reproductive, eye lens function and neural system development. However, the role of TBC1D20 on reproduction in female mice remain unclear. Methods: As a prospective laboratory-based study, a mouse model with spontaneous functional mutations of Tbc1d20 (Tbc1d20-/-) was employed to investigate the effect of Tbc1d20 on the fertility of female. Then the role of Tbc1d20 on postnatal female reproductive tract development and gonadal function was measured by immunohistochemistry assay and radioimmunoassay. A bilateral ovarian removal model and an artificial induced decidualization model were employed to reveal the function of Tbc1d20 on endometrial decidualization in vivo. Primary uterine stromal cells were isolated to evaluate the effect of Tbc1d20 on uterine stromal cell proliferation and the ability of decidualization in vitro. Results: Female Tbc1d20-/- mice were infertile. Functional mutations of Tbc1d20 exerted no obvious changes on the function of ovary, structure of fallopian tubes, and ability of early embryo implantation. However, Tbc1d20-/- mice presented marked reduction on the uterine size and weight at two-month-old, accompanied limitations on the myometrial thickness, the number of endometrial glands, and the density of blood vessels. Tbc1d20-/- mice exhibited an impaired uterine decidualization phenotype in vivo. In addition, in vitro primary cell model indicated that the proliferation and differentiation of uterine stromal cells were retarded while Tbc1d20 loss of function. Mechanically, TBC1D20 deficiency triggered endoplasmic reticulum stress in proliferating and differentiating uterine stromal cells. Conclusions: The findings from this study indicated that TBC1D20 is necessary for normal postnatal uterine development and endometrial decidualization in mice.https://www.imrpress.com/journal/CEOG/51/6/10.31083/j.ceog5106146tbc1d20uterine developmentdecidualizationendoplasmic reticulum stress |
| spellingShingle | Wenpeng Min Xi Li Jing Zhou Wei Yuan Qing Yang Xinmei Ji Bing Liu Liqiong Luo Yuxia He Lina Cui Wen-Lin Chang TBC1D20 is Essential for Postnatal Uterine Development and Endometrial Decidualization in Mice Clinical and Experimental Obstetrics & Gynecology tbc1d20 uterine development decidualization endoplasmic reticulum stress |
| title | TBC1D20 is Essential for Postnatal Uterine Development and Endometrial Decidualization in Mice |
| title_full | TBC1D20 is Essential for Postnatal Uterine Development and Endometrial Decidualization in Mice |
| title_fullStr | TBC1D20 is Essential for Postnatal Uterine Development and Endometrial Decidualization in Mice |
| title_full_unstemmed | TBC1D20 is Essential for Postnatal Uterine Development and Endometrial Decidualization in Mice |
| title_short | TBC1D20 is Essential for Postnatal Uterine Development and Endometrial Decidualization in Mice |
| title_sort | tbc1d20 is essential for postnatal uterine development and endometrial decidualization in mice |
| topic | tbc1d20 uterine development decidualization endoplasmic reticulum stress |
| url | https://www.imrpress.com/journal/CEOG/51/6/10.31083/j.ceog5106146 |
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