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Decidualization of human endometrial stromal cells (hESCs) is important for the maintenance of a successful pregnancy. Histone deacetylase 4 (HDAC4) was reported to be involved in the dysfunction of decidua-derived mesenchymal stem cells. However, the role of HDAC4 underlying decidualization of hESCs remains unclear. We intended to explore the function and molecular mechanism of HDAC4 in hESCs. In vitro expansion of hESCs using a serum-free medium was used to confirm the characteristics of hESCs. Gene expression in hESCs was evaluated by reverse transcription-quantitative polymerase chain reaction. CCK-8 assay, TUNEL staining, flow cytometry analysis, and Western blot analysis were performed to test the effects of HDAC4 and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on hESCs. RNA pull-down and luciferase reporter assays were performed to validate the relationship between genes. In this study, the characteristics of hESCs were sustained in serum-free medium during a process of propagation. HDAC4 knockdown suppressed hESCs viability and promoted hESCs apoptosis. HDAC4 was targeted by miR-498-3p in hESCs. MALAT1 bound with miR-498-3p in hESCs. HDAC4 expression was positively regulated by MALAT1 and negatively regulated by miR-498-3p in hESCs. HDAC4 upregulation countervailed the effects of MALAT1 silencing on hESCs proliferation, apoptosis, and decidualization of hESCs. Overall, MALAT1 facilitated the decidualization of hESCs via binding with miR-498-3p and upregulating HDAC4, which might provide a new direction for the maintenance of a successful pregnancy.

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Purpose Impaired decidualization contributes to the infertility in recurrent implantation failure (RIF). Herein, we focused on the function and probable mechanisms of miR-133b in endometrial stromal cells decidualization.Methods miR-133b and KLF12 protein levels in midsecretory endometrial tissues derived from women with and without RIF were measured by qRT-PCR and Western blot. Primary human endometrial stromal cells (HESCs) were isolated and cultured for in vitro decidualization assays. Luciferase reporter, qRT-PCR and Western blot assays were used to measure the relationship between miR-133b and KLF12.Results miR-133b was significantly downregulated, whereas KLF12 was upregulated in endometrial tissues from RIF. miR-133b effectively promoted HESCs in vitro decidualization through the modulation of KLF12 expression and the activation of LIF/STAT3 pathway. Conversely, inhibition of miR-133b expression reversed these effects. In addition, the luciferase reporter system demonstrated that miR-133b directly inhibited the expression of KLF12 by interacting with 3’ untranslated region of KLF12.Conclusion Our data suggest that miR-133b promotes HESCs decidualization by targeting KLF12 and reverses the impaired decidualization in RIF.

To assess the associations between mode of delivery and pregnancy outcomes in patients with intrahepatic cholestasis of pregnancy (ICP) based on the severity of maternal hypercholanemia. A hospital-based retrospective cohort study was performed between January 1, 2015, and December 31, 2019. Among the 177 women with mild total bile acids, 123 (69.5%) had a vaginal delivery and 54 (30.5%) underwent a cesarean delivery, of which 42 (23.7%) were planned and 12 (6.8%) were unplanned. Among the 50 severe ICP women, 13 (26.0%) had a vaginal delivery and 37 (74.0%) underwent a cesarean delivery, of which 26 (52.0%) were planned and 11 (22.0%) were unplanned. Severe ICP was associated with an increased risk of preterm delivery (P P=0.001), and neonatal intensive care unit admission (P

Background: Endometrial carcinoma (EC) still threatens the health of women. Thus, to explore how long intergenic non-protein coding RNA 01220 regulates the development of EC. Methods: Whole genome expression profile data of EC and paracancerous tissues in TCGA database were downloaded. LINC01220 expression in EC and paracancerous tissues of patients in our hospital were detected by qRT-PCR. Furthermore, the relationship between LINC01220 expression and clinicopathological features of EC patients was analyzed. After transfection with sh-LINC01220 and pcDNA-MAPK11 (mitogen-activated protein kinase) in EC cells, proliferative, colony formation abilities and apoptosis were determined by cell counting kit-8 (CCK-8), colony formation assay and flow cytometry, respectively. Western blot was conducted to determine the regulatory role of LINC01220 on MAPK11. Results: TCGA data showed that LINC01220 expression is markedly higher in EC tissues than that of paracancerous tissues, which was consistent without detection in EC patients of our hospital. LINC01220 expression was positively correlated to pathological grade and International Federation of Gynecology and Obstetrics (FIGO) stage of EC patients. After knockdown of LINC01220 in EC cells, proliferative and colony formation abilities decreased, whereas apoptotic rate increased. Cor function analysis revealed the positive correlation between LINC01220 and MAPK11 in EC. MAPK11 expression was regulated by LINC01220 in EC cells. Overexpression of MAPK11 can reverse the tumor suppressing effect of LINC01220 on EC. Conclusions: LINC01220 promotes EC development by stimulating proliferation and inhibiting apoptosis of EC cells through up-regulating MAPK11.

Successful embryonic implantation requires an effective maternal-embryonic molecular dialogue. However, the detailed mechanisms of epithelial-embryo adhesion remain poorly understood. Here, we report that matrix metalloproteinase-26 (MMP-26) is a novel downstream target gene of homeobox a 10 (HOXA10) in human endometrial cells. HOXA10 binds directly to a conserved TTAT unit (-442 to -439) located within the 5' regulatory region of the MMP-26 gene and regulates the expression and secretion of MMP-26 in a concentration-dependent manner. Moreover, the adenovirus-mediated overexpression of MMP-26 in Ishikawa cells markedly increased BeWo spheroid adhesion. An antibody blocking assay further demonstrated that the promotion of BeWo spheroid adhesion by HOXA10 and MMP-26 was significantly inhibited by pre-treatment with a specific antibody against MMP-26. These results demonstrate that the HOXA10-mediated expression of MMP-26 promotes embryo adhesion during the process of embryonic implantation.

Background Decidualization is a prerequisite for successful implantation and the establishment of pregnancy. Krüppel-like factor 12 (KLF12) is a negative regulator of endometrial decidualization in vitro. We investigated whether KLF12 was associated with impaired decidualization under conditions of repeated implantation failure (RIF). Methods Uterine tissues were collected from a mouse model of early pregnancy and artificial decidualization for immunohistochemistry, Western blot and real-time PCR analysis. Reporter gene assays, chromatin immunoprecipitation-PCR and avidin-biotin conjugate DNA precipitation assays were performed to analyze the transcriptional regulation of forkhead box O1 (FOXO1) by KLF12. Furthermore, the protein levels of KLF12 and FOXO1 in patients with RIF were analyzed by Western blot and immunohistochemistry. Results KLF12 led to defective implantation and decidualization in the mouse uterine model of early pregnancy and artificial decidualization by directly binding to the FOXO1 promoter region and inhibiting its expression in human endometrial stromal cells. Elevated KLF12 expression was accompanied by decreased FOXO1 expression in the endometria of patients with RIF. Conclusions As a novel regulator, KLF12 predominantly controls uterine endometrial differentiation during early pregnancy and leads to implantation failure. Electronic supplementary material The online version of this article (doi:10.1186/s12958-015-0079-z) contains supplementary material, which is available to authorized users.