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The objective of this study was to explore the regulation and function of CD55 in human decidualization. By immunohistochemical staining, it was found that CD55 expression was higher in first\u2010trimester decidua than in the endometrium. In both primary endometrial stromal cells and immortalized cell line T\u2010hESCs, CD55 was upregulated by induction of in vitro decidualization with medroxyprogesterone acetate (MPA) and 8\u2010Br\u2010cAMP. During decidualization in vitro, CD55\u00a0was stimulated by 8\u2010Br\u2010cAMP in a time\u2010 and concentration\u2010dependent manner, which was reversed by a PKA inhibitor H89 and partially by an AKT activator SC79. Knocking down CD55 expression diminished the expression of decidualization markers prolactin (<jats:italic>PRL<\/jats:italic>) and insulin\u2010like growth factor\u2010binding protein 1 (<jats:italic>IGFBP1<\/jats:italic>), accompanied by inhibition of Src, aberrant activation of ERK and decreased expression of several decidualization\u2010related genes, including <jats:italic>FOXO1<\/jats:italic>, <jats:italic>EGFR<\/jats:italic>, and <jats:italic>STAT3<\/jats:italic>. Furthermore, the decidua of unexplained miscarriage women and the endometrium of unexplained infertile women both exhibited decreased <jats:italic>CD55<\/jats:italic> expression. Collectively, these findings revealed that 8\u2010Br\u2010cAMP promotes CD55 expression via PKA activation and AKT dephosphorylation, and decreased CD55 impairs decidualization by inactivation of Src, aberrant activation of ERK pathway, and compromised expression of decidualization\u2010related genes, indicating that CD55 deficiency may contribute to the pathogenesis of spontaneous miscarriage and infertility.<\/jats:p>","DOI":"10.1002\/mrd.23569","type":"journal-article","created":{"date-parts":[[2022,4,27]],"date-time":"2022-04-27T04:56:25Z","timestamp":1651035385000},"page":"256-268","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["CD55 is upregulated by cAMP\/PKA\/AKT and modulates human decidualization via Src and ERK pathway and decidualization\u2010related genes"],"prefix":"10.1002","volume":"89","author":[{"given":"Zhijing","family":"Tang","sequence":"first","affiliation":[{"name":"Department of 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Fudan University Shanghai China"},{"name":"Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wingting","family":"Leung","sequence":"additional","affiliation":[{"name":"Department of Reproductive Endocrinology, Obstetrics and Gynecology Hospital Fudan University Shanghai China"},{"name":"Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiuying","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Reproductive Endocrinology, Obstetrics and Gynecology Hospital Fudan University Shanghai China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hexia","family":"Xia","sequence":"additional","affiliation":[{"name":"Department of Reproductive Endocrinology, Obstetrics and Gynecology Hospital Fudan University Shanghai 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