摘要：SummaryA conceptual framework for understanding abnormal endometrial decidualization, with considerable significance for the diagnosis and treatment of abnormal decidualization-related changes in non-receptive endometrium in implantation failure during early pregnancy is very important. Here, we found the expression levels of miR-29a in endometrial tissues were associated with the menstrual phases and pregnancy outcome. Inhibition of miR-29a led to decreased decidualization of endometrial stromal cells (ESCs)in vitro, whereas Tet methylcytosine dioxygenase 3 (TET3) and its potential demethylation target, the collagen type I alpha 1 chain (Col1A1), were restored. The binding capacity of TET3 to the Col1A1 promoter could be enhanced by the inhibition of miR-29a. Finally, deletion of TET3 rescued the inhibitory effect of the miR-29a antagomir on the proliferation of decidualized ESCsin vitroand embryo implantationin vivo. Thus, loss of miR-29a causes implantation failure because of the limitation of ESCs decidualization-related changes in non-receptive endometrium during early pregnancy.Graphical abstractDisplay OmittedHighlights•Loss of miR-29a inhibits decidualization of ESCs•TET3 demethylates the Col1A1 promoter•Loss of miR-29a enhances the binding capacity of TET3 to the Col1A1 promoter•Loss of miR-29a suppresses embryo implantation during early pregnancy in miceMolecular biology; Cell biology; Developmental biology
