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Estrogen restricts the apoptosis of endometrial stromal cells by promoting TSLP secretion.
Yang, Hui-Li; Chang, Kai-Kai; Mei, Jie; Zhou, Wen-Jie; Liu, Li-Bing; Yao, Li; Meng, Yi; Wang, Ming-Yan; Ha, Si-Yao; Lai, Zhen-Zhen; Ye, Jiang-Feng; Li, Da-Jin; Li, Ming-Qing.
Affiliation
  • Yang HL; Laboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai 200080, P.R. China.
  • Chang KK; Department of Gynecology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai 200011, P.R. China.
  • Mei J; Department of Obstetrics and Gynecology, Reproductive Medicine Center, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medicine School, Nanjing, Jiangsu 210000, P.R. China.
  • Zhou WJ; Laboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai 200080, P.R. China.
  • Liu LB; Department of Gynecology, Changzhou No. 2 People's Hospital, Affiliated with Nanjing Medical University, Changzhou, Jiangsu 213003, P.R. China.
  • Yao L; Laboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai 200080, P.R. China.
  • Meng Y; Department of Clinical Laboratory, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai 200011, P.R. China.
  • Wang MY; Department of Clinical Laboratory, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai 200011, P.R. China.
  • Ha SY; Laboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai 200080, P.R. China.
  • Lai ZZ; Laboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai 200080, P.R. China.
  • Ye JF; Department of Clinical Epidemiology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai 200011, P.R. China.
  • Li DJ; Laboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai 200080, P.R. China.
  • Li MQ; Laboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai 200080, P.R. China.
Mol Med Rep ; 18(5): 4410-4416, 2018 Nov.
Article in En | MEDLINE | ID: mdl-30152851
ABSTRACT
Endometriosis (EMS) is a female hormone­ dependent disease with controversial reports of its etiology and pathogenesis. Apoptosis is particularly important in the human endometrium due to the dynamic cycles of proliferation and shedding. Estrogen possessed antiapoptotic effects on endometrial stromal cells (ESCs), which appears to be exacerbated in women with EMS; however, the underlying mechanism of the antiapoptotic effects of estrogen on ESC remains unknown. The present study aimed to determine whether estrogen regulates the apoptosis of ESCs via thymic stromal lymphopoietin (TSLP) and the associated mechanism. An ELISA was conducted to detect TSLP content in the ESC culture medium treated with estrogen. Subsequently, the early apoptotic rate and expression of B­cell lymphoma (Bcl­2) of ESCs were analyzed by flow cytometry in the presence of recombinant human TSLP, anti­human TSLP neutralizing antibody or estrogen. In the present study, it was reported that ESCs exhibited basal TSLP secretion in the absence of estrogen as reported in previous studies, and that estrogen promoted TSLP secretion of ESCs in a dose­dependent manner. The results demonstrated that estrogen suppressed the apoptosis of ESCs associated with the promotion of Bcl­2 expression, which may be partly reversed by inhibiting TSLP. Therefore, the findings of the present study revealed a novel mechanism of estrogen­dependent apoptotic suppression of ESCs associated with TSLP secretion and Bcl­2 regulation. Endogenous and estrogen­induced endometrial TSLP may promote the initiation and development of EMS via the inhibition of apoptosis.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Cytokines / Proto-Oncogene Proteins c-bcl-2 / Cell Proliferation / Endometriosis Limits: Adult / Female / Humans / Middle aged Language: En Journal: Mol Med Rep Year: 2018 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Cytokines / Proto-Oncogene Proteins c-bcl-2 / Cell Proliferation / Endometriosis Limits: Adult / Female / Humans / Middle aged Language: En Journal: Mol Med Rep Year: 2018 Document type: Article
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