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      Inhibition of TMEM16A impedes embryo implantation and decidualization in mice.

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          Abstract

          Recent studies revealed that TMEM16A is involved in several reproductive processes, including ovarian estrogen secretion and ovulation, sperm motility and acrosome reaction, fertilization and myometrium contraction. However, little is known about the expression and function of TMEM16A in embryo implantation and decidualization. In this study, we focused on the expression and regulation of TMEM16A in mouse uterus during early pregnancy. We found that TMEM16A is upregulated in uterine endometrium in response to embryo implantation and decidualization. Progesterone treatment could induce TMEM16A expression in endometrial stromal cells through progesterone receptor/c-Myc pathway, which is blocked by progesterone receptor antagonist or the inhibitor of c-Myc signaling pathway. Inhibition of TMEM16A by small molecule inhibitor (T16Ainh-A01) resulted in impaired embryo implantation and decidualization in mice. Treatment with either specific siRNA of Tmem16a or T16Ainh-A01 inhibited the decidualization and proliferation of mouse endometrial stromal cells. In conclusion, our results revealed that TMEM16A is involved in embryo implantation and decidualization in mice, compromised function of TMEM16A may lead to impaired embryo implantation and decidualization.

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          Author and article information

          Journal
          Reproduction
          Reproduction (Cambridge, England)
          Bioscientifica
          1741-7899
          1470-1626
          December 2018
          : 156
          : 6
          Affiliations
          [1 ] Center for Reproductive Medicine, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
          [2 ] Medical College of Wuhan University, Wuhan, People's Republic of China.
          Article
          REP-18-0197
          10.1530/REP-18-0197
          30328351
          47111263-f229-4b1d-9ecc-bfbde8c653a5

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