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Wenqian Xiong Department of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China

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Ling Zhang Department of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China

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Lan Yu Department of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China

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Wei Xie Department of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China

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Yicun Man Department of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China

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Yao Xiong Department of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China

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Hengwei Liu Department of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China

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Yi Liu Department of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China
Department of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Tongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China

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Endometriosis is an estrogen-dependent disease that involves the adhesion, invasion, and angiogenesis of endometrial tissues outside of the uterine cavity. We hypothesized that a link exists between estrogen and beta-catenin (β-catenin) signaling in the pathogenesis of endometriosis. Human endometrial stromal cells (HESCs) were separated from eutopic endometrial tissues that were obtained from patients with endometriosis. β-catenin expression and cells invasiveness ability were up-regulated by 17β-estradiol (E2) in an estrogen receptor (ESR)-dependent manner, whereas β-catenin siRNA abrogated this phenomenon. Moreover, co-immunoprecipitation and dual immunofluorescence studies confirmed ESR1, β-catenin, and lymphoid enhancer factor 1/T cell factor 3 co-localization in the nucleus in HESCs after E2 treatment. To determine the role of β-catenin signaling in the implantation of ectopic endometrium, we xenotransplanted eutopic endometrium from endometriosis patients into ovariectomized severe combined immunodeficiency mice. The implantation of the endometrium was suppressed by β-catenin siRNA. Collectively, studies regarding β-catenin signaling are critical for improving our understanding of the pathogenesis of estrogen-induced endometriosis, which can translate into the development of treatments and therapeutic strategies for endometriosis.

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Na Li Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Ling Zhang Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Qi Li Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Yu Du Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Hengwei Liu Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Yi Liu Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Wenqian Xiong Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Oestrogen has been reported to control the invasiveness of endometrial stromal cells in endometriosis. Notch signalling, a master regulator of cell invasion in tumours, is regulated by oestrogen in other diseases and hyperactivated in endometriotic stromal cells. Therefore, we hypothesized that an interaction between Notch signalling and oestrogen may exist in the regulation of endometrial stromal cell invasion, which is essential for the development of endometriosis. Western blot analysis of tissues showed that the expression levels of Notch components (JAG1 and NOTCH1) and Notch activity were markedly higher in ectopic endometria than in their eutopic and normal counterparts. Primary stromal cells obtained from normal endometria cultured with oestrogen presented significant increases in the expression of Notch components and Notch activity, the cytoplasmic and nuclear accumulation of NOTCH1 intracellular domain, the expression of matrix metallopeptidase 9 and vascular endothelial growth factor and cell invasiveness. Knockdown of NOTCH1 markedly alleviated oestrogen-induced matrix metallopeptidase 9 and vascular endothelial growth factor expression and cell invasion. ICI (an oestrogen receptor α antagonist) also blocked these oestrogenic effects. Oestrogen-responsive elements were found in the promoters of NOTCH1 and JAG1. A luciferase reporter analysis revealed that oestrogen regulated the expression of Notch components via oestrogen receptor alpha, which is bound to oestrogen-responsive elements in the JAG1 and NOTCH1 promoters. Collectively, our findings indicate that oestrogen engages in crosstalk with Notch signalling to regulate cell invasion in endometriosis via the activation of oestrogen receptor alpha and the enhancement of Notch activity. Notch signalling blockade may therefore be a novel therapeutic target for endometriosis.

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Hengwei Liu Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Zhibing Zhang Department of Obstetrics and Gynecology, Virginia Commonwealth University, Richmond, Virginia, USA

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Wenqian Xiong Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Ling Zhang Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Yao Xiong Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Na Li Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Haitang He Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Yu Du Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Yi Liu Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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Endometriosis is a benign gynecological disease that shares some characteristics with malignancy like migration and invasion. It has been reported that both hypoxia-inducible factor-1α (HIF-1α) and autophagy were upregulated in ectopic endometrium of patients with ovarian endometriosis. However, the crosstalk between HIF-1α and autophagy in the pathogenesis of endometriosis remains to be clarified. Accordingly, we investigated whether autophagy was regulated by HIF-1α, as well as whether the effect of HIF-1α on cell migration and invasion is mediated through autophagy upregulation. Here, we found that ectopic endometrium from patients with endometriosis highly expressed HIF-1α and autophagy-related protein LC3. In cultured human endometrial stromal cells (HESCs), autophagy was induced by hypoxia in a time-dependent manner and autophagy activation was dependent on HIF-1α. In addition, migration and invasion ability of HESCs were enhanced by hypoxia treatment, whereas knockdown of HIF-1α attenuated this effect. Furthermore, inhibiting autophagy with specific inhibitors and Beclin1 siRNA attenuated hypoxia triggered migration and invasion of HESCs. Taken together, these results suggest that HIF-1α promotes HESCs invasion and metastasis by upregulating autophagy. Thus, autophagy may be involved in the pathogenesis of endometriosis and inhibition of autophagy might be a novel therapeutic approach to the treatment of endometriosis.

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Yu Du Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China
Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China

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Zhibing Zhang Department of Physiology and Obstetrics and Gynecology, Wayne State University, Detroit, Michigan, USA

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Wenqian Xiong Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

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Na Li Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

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Hengwei Liu Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

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Haitang He Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

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Qi Li Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

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Yi Liu Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

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Ling Zhang Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

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Endometriosis is an estrogen-dependent benign gynecological disease that shares some common features of malignancy. Epithelial–mesenchymal transition (EMT) has been recognized as a core mechanism of endometriosis. MALAT1 is widely known as EMT promoter, while miR200 family members (miR200s) are considered as EMT inhibitors. Previous studies have reported that MALAT1 upregulation and miR200s downregulation are observed in endometriosis. MiR200c has been regarded as the strongest member of miR200s to interact with MALAT1. However, whether MALAT1/miR200c regulates EMT remains largely unclear. In this study, the roles of miR200s and MALAT1 in ectopic endometrium were investigated. Additionally, the effects of E2 on EMT and MALAT1/miR200s were examined in both EECs and Ishikawa cells. Notably, E2 could upregulate MALAT1 and downregulate miR200s expression levels and induce EMT in EECs and Ishikawa cells. PHTPP, an ERβ antagonist, could reverse the effect of E2. Overexpression of miR200c and knockdown of MALAT1 significantly inhibited E2-mediated EMT, suggesting that both miR200c and MALAT1 are involved in the E2-induced EMT process in endometriosis. In addition, a reciprocal inhibition was found between miR200s and MALAT1. Therefore, the role of MALAT1/miR200c in EMT is influenced by the presence of estrogen during endometriosis development.

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Antonia Otoo Department of Obstetrics and Gynecology, Women and Children's Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
Department of Reproductive Biology, Joint International Research Laboratory of Reproduction and Development, School of Public Health, Chongqing Medical University, Chongqing, People’s Republic of China

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Armin Czika Department of Reproductive Biology, Joint International Research Laboratory of Reproduction and Development, School of Public Health, Chongqing Medical University, Chongqing, People’s Republic of China
Research and Development Institute, Faculty of Medicine, Transilvania University of Brasov, Brasov, Romania

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Jones Lamptey Department of Reproductive Biology, Joint International Research Laboratory of Reproduction and Development, School of Public Health, Chongqing Medical University, Chongqing, People’s Republic of China

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Jun-Pu Yang Department of Reproductive Biology, Joint International Research Laboratory of Reproduction and Development, School of Public Health, Chongqing Medical University, Chongqing, People’s Republic of China

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Qian Feng Department of Gynecology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, People’s Republic of China

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Mei-Jiao Wang Department of Reproductive Biology, Joint International Research Laboratory of Reproduction and Development, School of Public Health, Chongqing Medical University, Chongqing, People’s Republic of China
Department of Physiology, School of Basic Medical Science, Chongqing Medical University, Chongqing, People’s Republic of China

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Ying-Xiong Wang Department of Obstetrics and Gynecology, Women and Children's Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
Department of Reproductive Biology, Joint International Research Laboratory of Reproduction and Development, School of Public Health, Chongqing Medical University, Chongqing, People’s Republic of China

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Yu-Bin Ding Department of Obstetrics and Gynecology, Women and Children's Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
Department of Reproductive Biology, Joint International Research Laboratory of Reproduction and Development, School of Public Health, Chongqing Medical University, Chongqing, People’s Republic of China
Department of Pharmacology, Academician Workstation, Changsha Medical University, Changsha, China

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In brief

Obese PCOS mice display metabolic and endocrine disorders that manifest as abnormal metabolism of glucose and dysfunctions in the reproductive system. This study demonstrates that emodin alleviates most of these conditions possibly via the HMGB1/TLR4/NF-kB pathway.

Abstract

PCOS is a reproductive disorder with an unclear etiology. It affects 5–10% of women worldwide and is largely associated with impaired glucose metabolism and obesity. HMGB1 is a nuclear protein associated with impaired glucose metabolism and PCOS. We sought to investigate the potential therapeutic effects of emodin on glucose metabolism and ovarian functions in PCOS mice via the HMGB1 molecular pathway. A high-fat diet (HFD) and dehydroepiandrosterone (DHEA)- induced PCOS mouse model comprising four experimental groups was established: control, PCOS, PCOS plus emodin, and PCOS plus vehicle groups. Emodin administration attenuated obesity, elevated fasting glucose levels, impaired glucose tolerance, and insulin resistance, and improved the polycystic ovarian morphology of PCOS mice. Additionally, it lowered elevated serum HMGB1, LH, and testosterone levels in PCOS mice. Elevated ovarian protein and mRNA levels of HMGB1 and TLR4 in PCOS mice were also lowered following emodin treatment. Furthermore, emodin lowered high NF-ĸB/65 protein levels in the ovaries of PCOS mice. Immunohistochemical staining of the ovaries revealed strong HMGB1, TLR4, and AR expressions in PCOS mice, which were lowered by emodin treatment. Moreover, emodin significantly increased GLUT4, IRS2, and INSR levels that were lowered by PCOS. Overall, our study showed that emodin alleviated the impaired glucose metabolism and improved ovarian function in PCOS mice, possibly via the HMGB1/TLR4/NF-ĸB signaling pathway. Thus, emodin could be considered a potential therapeutic agent in the management of PCOS.

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Wang Han-zheng
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Lu Shu-hua
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Shen Wei-xiong
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Sun Zhi-da
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Zhou Wei
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Wu Yu-fen
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Zhou Mei-rong
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Summary. Cell suspensions were prepared from human corpora lutea obtained during the mid-luteal phase. Progesterone production was assessed after short-term incubation of luteal cell suspensions. Luteal cells were very sensitive to hCG, the concentration required for 50% maximum response being 0·01 i.u./ml, and the response was 5 times higher than the basal production.

Oestradiol (1–100 μm) induced a significant dose-related decrease in both basal and hCG-stimulated progesterone production. The A-nor steroidal compounds anordrin and AF-45 reduced hCG-stimulated progesterone production only at the high concentration of 100 μm. The ED50 values were approximately 3 μm, 75 μm and 100 μm for oestradiol, AF-45 and anordrin respectively. Anordrin showed no significant effects on basal progesterone production. In addition, oestradiol markedly inhibited the activity of 3β-hydroxysteroid dehydrogenase in luteal cells, expressed by the conversion of pregnenolone to progesterone, but the inhibitory effects of anordrin and AF-45 were negligible or relatively low.

The effects of anordrin and AF-45 were different from those of oestradiol on progesterone production by human luteal cells in vitro, indicating that neither substance is likely to be a useful luteolytic agent in women.

Keywords: A-nor steroid; oestradiol; luteal cells; progesterone; 3β-hydroxysteroid dehydrogenase; man

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Yuansong Yu Department of Cell Biology, College of Life Sciences, Beijing University, Beijing 100871, China, Beijing Laboratory Animal Research Center, Beijing 100012, China and College of Animal Science and Technology, Agricultural University of Hebei, Baoding 071001, China

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Jun Yong Department of Cell Biology, College of Life Sciences, Beijing University, Beijing 100871, China, Beijing Laboratory Animal Research Center, Beijing 100012, China and College of Animal Science and Technology, Agricultural University of Hebei, Baoding 071001, China

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Xiangyun Li Department of Cell Biology, College of Life Sciences, Beijing University, Beijing 100871, China, Beijing Laboratory Animal Research Center, Beijing 100012, China and College of Animal Science and Technology, Agricultural University of Hebei, Baoding 071001, China

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Tingting Qing Department of Cell Biology, College of Life Sciences, Beijing University, Beijing 100871, China, Beijing Laboratory Animal Research Center, Beijing 100012, China and College of Animal Science and Technology, Agricultural University of Hebei, Baoding 071001, China

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Han Qin Department of Cell Biology, College of Life Sciences, Beijing University, Beijing 100871, China, Beijing Laboratory Animal Research Center, Beijing 100012, China and College of Animal Science and Technology, Agricultural University of Hebei, Baoding 071001, China

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Xiaoran Xiong Department of Cell Biology, College of Life Sciences, Beijing University, Beijing 100871, China, Beijing Laboratory Animal Research Center, Beijing 100012, China and College of Animal Science and Technology, Agricultural University of Hebei, Baoding 071001, China

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Jiefang You Department of Cell Biology, College of Life Sciences, Beijing University, Beijing 100871, China, Beijing Laboratory Animal Research Center, Beijing 100012, China and College of Animal Science and Technology, Agricultural University of Hebei, Baoding 071001, China

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Mingxiao Ding Department of Cell Biology, College of Life Sciences, Beijing University, Beijing 100871, China, Beijing Laboratory Animal Research Center, Beijing 100012, China and College of Animal Science and Technology, Agricultural University of Hebei, Baoding 071001, China

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Hongkui Deng Department of Cell Biology, College of Life Sciences, Beijing University, Beijing 100871, China, Beijing Laboratory Animal Research Center, Beijing 100012, China and College of Animal Science and Technology, Agricultural University of Hebei, Baoding 071001, China

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In this study, we cloned mice from ES cells by a post-electrofusion MG132 treatment and improved development of cloned embryos with a sequential cultivation protocol. When 5 μM MG132, a proteasome inhibitor, were used to treat the reconstructed embryos, the capacity of in vitro development, implantation and full-term development were significantly improved. Blastocyst formation rates of the reconstructed embryos from X4 ES cells (F1 strain derived from C57BL/6 × 129sv) and J1 ES cells obtained with or without MG132 treatment were 66.9% and 26.6%, and 66.1% and 34.5% respectively (P < 0.05). A total of 146 two-cell embryos cloned from X4 ES cells with MG132 treatment were transferred to recipients, and five cloned pups (3.4%) were born, of which four survived. When the same numbers of two-cell embryos cloned from X4 ES cells without MG132 treatment were transferred, however, no live-born mice were obtained. When embryos cloned from J1 ES cells without MG132 treatment were cultured in KSOM medium for 54 h followed by culture in CZB medium containing 5.6 mM glucose for 42 h, the blastocyst rate was significantly higher than when they were cultured in KSOM continuously for 96 h (34.5% vs 17.1%). However, sequential cultivation did not improve the development of embryos cloned with MG132 treatment and that of parthenotes. In conclusion, MG132 treatment increased the developmental potential of reconstructed mouse embryos, and sequential cultivation improved development of the embryos cloned by electrofusion without MG132 treatment.

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Xue-Yun Qin Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Fudan University, Shanghai, People’s Republic of China

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Hui-Hui Shen Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Fudan University, Shanghai, People’s Republic of China

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Xin-Yan Zhang Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China

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Xing Zhang Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China

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Feng Xie Center for Diagnosis and Treatment of Cervical and Uterine Diseases, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China

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Wen-Jun Wang Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China

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Yu Xiong Department of Obstetrics, Hospital of Obstetrics and Gynecology, Shanghai Medical School, Fudan University, Shanghai, People’s Republic of China
Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China

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Jie Mei Reproductive Medicine Center, Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medicine School, Nanjing, People’s Republic of China

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Ming-Qing Li Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China
NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Fudan University, Shanghai, People’s Republic of China
Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai, People’s Republic of China

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In brief

Hypoxia is vital for the establishment of the maternal–fetal interface during early pregnancy. This study shows that decidual macrophages (dMφ) could be recruited and reside in decidua under the regulation of hypoxia/VEGFA-CCL2 axis.

Abstract

Infiltration and residence of decidual macrophages (dMφ) are of great significance to pregnancy maintenance for their role in angiogenesis, placental development, and inducing immune tolerance. Besides, hypoxia has now been acknowledged as an important biological event at maternal–fetal interface in the first trimester. However, whether and how hypoxia regulates biofunctions of dMφ remain elusive. Herein, we observed increased expression of C–C motif chemokine ligand 2 (CCL2) and residence of macrophages in decidua compared to secretory-phase endometrium. Moreover, hypoxia treatment on stromal cells improved the migration and adhesion of dMφ. Mechanistically, these effects might be mediated by upregulated CCL2 and adhesion molecules (especially ICAM2 and ICAM5) on stromal cells in the presence of endogenous vascular endothelial growth factor-A (VEGFA) in hypoxia. These findings were also verified by recombinant VEGFA and indirect coculture, indicating that the interaction between stromal cells and dMφ in hypoxia condition may facilitate dMφ recruitment and residence. In conclusion, VEGFA derived from a hypoxic environment may manipulate CCL2/CCR2 and adhesion molecules to enhance the interactions between dMφ and stromal cells and thus contribute to the enrichment of macrophages in decidua early during normal pregnancy.

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Xue Zhang Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, People’s Republic of China
The Joint International Research Laboratory of Reproduction and Development, Ministry of Education, Chongqing Medical University, Chongqing, People’s Republic of China

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Bo-Yin Tan Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, People’s Republic of China
The Joint International Research Laboratory of Reproduction and Development, Ministry of Education, Chongqing Medical University, Chongqing, People’s Republic of China

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Shuang Zhang The Joint International Research Laboratory of Reproduction and Development, Ministry of Education, Chongqing Medical University, Chongqing, People’s Republic of China

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Qian Feng Department of Gynecology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, People’s Republic of China

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Ying Bai Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, People’s Republic of China

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Shi-Quan Xiao Department of Reproductive Medicine, The Third affiliated hospital of Chongqing Medical University, Chongqing, People’s Republic of China

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Xue-Mei Chen Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, People’s Republic of China
The Joint International Research Laboratory of Reproduction and Development, Ministry of Education, Chongqing Medical University, Chongqing, People’s Republic of China

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Jun-Lin He Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, People’s Republic of China
The Joint International Research Laboratory of Reproduction and Development, Ministry of Education, Chongqing Medical University, Chongqing, People’s Republic of China

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Xue-Qing Liu Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, People’s Republic of China
The Joint International Research Laboratory of Reproduction and Development, Ministry of Education, Chongqing Medical University, Chongqing, People’s Republic of China

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Ying-Xiong Wang Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, People’s Republic of China
The Joint International Research Laboratory of Reproduction and Development, Ministry of Education, Chongqing Medical University, Chongqing, People’s Republic of China

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Yu-Bin Ding Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, People’s Republic of China
The Joint International Research Laboratory of Reproduction and Development, Ministry of Education, Chongqing Medical University, Chongqing, People’s Republic of China

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Fang-Fang Li Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, People’s Republic of China
The Joint International Research Laboratory of Reproduction and Development, Ministry of Education, Chongqing Medical University, Chongqing, People’s Republic of China

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Decidualization of uterine stromal cells plays an important role in the establishment of normal pregnancy. Previous studies have demonstrated that Acyl-CoA binding protein (Acbp) is critical to cellular proliferation, differentiation, mitochondrial functions, and autophagy. The characterization and physiological function of Acbp during decidualization remain largely unknown. In the present study, we conducted the expression profile of Acbp in the endometrium of early pregnant mice. With the occurrence of decidualization, the expression of Acbp gradually increased. Similarly, Acbp expression was also strongly expressed in decidualized cells following artificial decidualization, both in vivo and in vitro. We applied the mice pseudopregnancy model to reveal that the expression of Acbp in the endometrium of early pregnant mice was not induced by embryonic signaling. Moreover, P4 significantly upregulated the expression of Acbp, whereas E2 appeared to have no regulating effect on Acbp expression in uterine stromal cells. Concurrently, we found that interfering with Acbp attenuated decidualization, and that might due to mitochondrial dysfunctions and the inhibition of fatty acid oxidation. The level of autophagy was increased after knocking down Acbp. During induced decidualization, the expression of ACBP was decreased with the treatment of rapamycin (an autophagy inducer), while increased with the addition of Chloroquine (an autophagy inhibitor). Our work suggests that Acbp plays an essential role in the proliferation and differentiation of stromal cells during decidualization through regulating mitochondrial functions, fatty acid oxidation, and autophagy.

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Xue-Ying Zhang The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education, Hangzhou, Zhejiang, China

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Yi-Meng Xiong The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education, Hangzhou, Zhejiang, China

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Ya-Jing Tan The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Li Wang The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Rong Li The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Yong Zhang The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Xin-Mei Liu The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Xian-Hua Lin The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Li Jin The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Yu-Ting Hu The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Zhen-Hua Tang The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Zheng-Mu Wu The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Feng-Hua Yin The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Zheng-Quan Wang The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Ye Xiao The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Jian-Zhong Sheng The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education, Hangzhou, Zhejiang, China
Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China

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He-Feng Huang The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education, Hangzhou, Zhejiang, China
The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
Shanghai Key Laboratory of Embryo Original Diseases, Shanghai, China

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Fertilization failure often occurs during in vitro fertilization (IVF) cycles despite apparently normal sperm and oocytes. Accumulating evidence suggests that mitochondria play crucial roles in the regulation of sperm function and male fertility. 3-Nitrophthalic acid (3-NPA) can induce oxidative stress in mitochondria, and melatonin, as an antioxidant, can improve mitochondrial function by reducing mitochondrial oxidative stress. The role of sperm mitochondrial dysfunction in fertilization failure during IVF is unclear. The present study revealed that spermatozoa with low, or poor, fertilization rates had swollen mitochondria, increased mitochondria-derived ROS, and attenuated mitochondrial respiratory capacity. 3-NPA treatment enhanced mitochondrial dysfunction in sperm. Spermatozoa with poor fertilization rates, and spermatozoa treated with 3-NPA, had reduced penetration ability. The concentration of melatonin was decreased in semen samples with low and poor fertilization rates. Melatonin, not only decreased excessive mitochondria-derived ROS, but also ‘rescued’ the reduced penetration capacity of spermatozoa treated with 3-NPA. Taken together, the study suggested that mitochondria-derived ROS and mitochondrial respiratory capacity are independent bio-markers for sperm dysfunction, and melatonin may be useful in improving sperm quality and overall male fertility.

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