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dc.contributor.authorWu Jinxiang
dc.contributor.authorKong Shuangbo
dc.contributor.authorGuo Chuanhui
dc.contributor.authorWang Jianqi
dc.contributor.authorLu Jinhua
dc.contributor.authorJiang Ruiwei
dc.contributor.authorWang Haibin
dc.date.accessioned2020-10-10T02:09:19Z
dc.date.available2020-10-10T02:09:19Z
dc.date.issued2019-12-11
dc.identifier.citationReproductive toxicology (Elmsford, N.Y.),2019,
dc.identifier.other10.1016/j.reprotox.2019.09.003
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/174831
dc.description.abstractOur understanding of the relationship between stress-derived epinephrine and early pregnancy failure remains incomplete. Here, we explored the effect of epinephrine exposure on early pregnancy and pseudopregnancy in mice. Increased expression of adrenergic receptors Adra1b, Adra2b and Adrb2 was observed during decidualization and post-implantation embryogenesis was delayed or survival impaired. Epinephrine treatment also impaired decidualization in both the gravid and pseudopregnant uterus, suggesting the effect on decidualization was independent of the conceptus. This included a suppression of endometrial stroma cell proliferation and of key decidualization regulators, including COX2, BMP2 and WNT4. Collectively, these data demonstrate that maternal epinephrine exposure during early pregnancy impairs uterine decidualization and embryo development, underlying early pregnancy failure.
dc.language.isozh_CN
dc.subjectDecidualization
dc.subjectEpinephrine
dc.subjectPregnancy failure
dc.subjectStress
dc.titleAn exaggerated epinephrine-adrenergic receptor signaling impairs uterine decidualization in mice.
dc.typeArticle


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