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Sha Peng State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and
State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Jing Li State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and
State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Chenglin Miao State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and
State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Liwei Jia State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and
State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Zeng Hu State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and
State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Ping Zhao State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and
State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Juxue Li State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and
State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Ying Zhang State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and
State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Qi Chen State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and
State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Enkui Duan State Key Laboratory of Reproductive Biology, Graduate School of the Chinese Academy of Sciences, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, China and

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Dickkopf-1 (Dkk1) is one of the secreted antagonists in the canonical Wnt signaling pathway. It plays important roles in diverse developmental processes. However, the role of Dkk1 in trophoblast cell invasion during placentation remains unclear. In this study, we found that Dkk1 was mainly expressed in maternal decidual tissue but trivially in ectoplacental cones (EPCs) in day 8 post coitum (p.c.) pregnant mouse uterus and that the efficiency of EPC attachment and outgrowth was increased when co-cultured with decidual cells, which secreted Dkk1, and this enhancement was abolished by pretreating decidual cells with Dkk1 blocking antibody before co-culture experiment. This indicates that Dkk1 secreted by decidual cells plays an important role in trophoblast cell invasion. Indeed, when recombinant mouse Dkk1 was added to EPCs in vitro, the efficiency of attachment and outgrowth was increased. Migration of EPCs toward the decidua was retarded when antisense Dkk1 oligonucleotide (ODN) was administered via intrauterine injection in vivo. Furthermore, the active β-catenin nuclear location was lost when we treated cultured EPCs with recombinant mouse Dkk1, and the efficiency of EPCs attachment and outgrowth was obviously increased when we treated cultured EPCs with antisense β-catenin ODN. Taken together, Dkk1 secreted by decidual cells may induce trophoblast cell invasion in the mouse and β-catenin may be involved in such functions of Dkk1.

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Hong-Jie Yuan Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai’an City, People’s Republic of China

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Zhi-Bin Li Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai’an City, People’s Republic of China

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Xin-Yue Zhao Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai’an City, People’s Republic of China

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Guang-Yi Sun Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai’an City, People’s Republic of China

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Guo-Liang Wang Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai’an City, People’s Republic of China

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Ying-Qi Zhao Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai’an City, People’s Republic of China

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Min Zhang Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai’an City, People’s Republic of China

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Jing-He Tan Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai’an City, People’s Republic of China

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Mechanisms by which female stress and particularly glucocorticoids impair oocyte competence are largely unclear. Although one study demonstrated that glucocorticoids triggered apoptosis in ovarian cells and oocytes by activating the FasL/Fas system, other studies suggested that they might induce apoptosis through activating other signaling pathways as well. In this study, both in vivo and in vitro experiments were conducted to test the hypothesis that glucocorticoids might trigger apoptosis in oocytes and ovarian cells through activating the TNF-α system. The results showed that cortisol injection of female mice (1.) impaired oocyte developmental potential and mitochondrial membrane potential with increased oxidative stress; (2.) induced apoptosis in mural granulosa cells (MGCs) with increased oxidative stress in the ovary; and (3.) activated the TNF-α system in both ovaries and oocytes. Culture with corticosterone induced apoptosis and activated the TNF-α system in MGCs. Knockdown or knockout of TNF-α significantly ameliorated the pro-apoptotic effects of glucocorticoids on oocytes and MGCs. However, culture with corticosterone downregulated TNF-α expression significantly in oviductal epithelial cells. Together, the results demonstrated that glucocorticoids impaired oocyte competence and triggered apoptosis in ovarian cells through activating the TNF-α system and that the effect of glucocorticoids on TNF-α expression might vary between cell types.

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