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Hyperglycemia in pregnancy (HIP) is linked to fetoplacental endothelial dysfunction, which might be a result of hyperglycemia. Hyperglycemia is associated with cell senescence; however, the role and mechanism of high glucose and cell senescence in HIP endothelial cell failure are largely unknown. Our study discovered that human umbilical vein endothelial cells (HUVECs) obtained from HIP pregnant women exhibit excessive senescence, with significantly elevated expression of senescence markers senescence-associated beta-galactosidase (SA-β-gal), p16, p21, and p53. Subsequently, we found that exposing primary HUVECs and cell lines to high glucose resulted in an increase in the synthesis of these senescence indicators, similar to what had been observed in pregnant women with HIP. A replicate senescence model and stress-induced premature senescence (SIPS) model showed higher amounts of vascular damage indicators, including von Willebrand factor (vWF), chemotactic C-C motif chemokine ligand 2 (CCL2), intercellular adhesion molecule 1 (ICAM-1), along with the anti-apoptotic protein BCL2. However, lower expressions of the pro-apoptotic component BAX, in addition to defective proliferation and tubulogenesis, were seen. Further studies indicated that hyperglycemia can not only induce these alterations in HUVECs but also exacerbate the aforementioned changes in both aging HUVECs. The experiments outlined above have also been validated in pregnant women with HIP. Collectively, these data suggest that exposure to high glucose accelerates cell senescence-mediated vein endothelial cell dysfunction, including excessive inflammation, cell adhesion, impaired angiogenesis, and cell proliferation possibly contributing to pregnancy complications and adverse pregnancy outcomes. [ABSTRACT FROM AUTHOR]

Tubal ectopic pregnancy (TEP) occurs when an embryo aberrantly implants in the fallopian tube, leading to abortive or ruptured tubal ectopic pregnancy (AEP or REP). Poor outcomes of REP include maternal infertility or mortality. Current studies on the prevention and treatment of ruptured tubal ectopic pregnancy (REP) are unfortunately hampered by a lack of the cell spectrum and cell–cell communications in the maternal–foetal interface. Here, we investigate the mechanisms of tubal rupture through single‐cell transcriptome profiling of the fallopian tube‐trophoblast interface in REP, AEP and intrauterine pregnancy patients. In REP, extravillous trophoblast (EVTs) cells form a dominant cell population, displaying aggressive invasion and proliferation, with robust differentiation into three subsets. Cell communication analysis identified colony‐stimulating factor 1 (CSF1), overexpressed by fallopian tube secretory epithelial cells in REP, with CSF1R on EVTs and macrophages, as a ligand/receptor pair that stimulates EVT invasion and macrophage accumulation. CSF1+ secretory epithelial cells stimulate EVTs migration and invasion, leading to a tubal rupture in REP. These results provide a mechanistic context and cellular milieu leading to tubal rupture, facilitating further study and development of therapeutics for REP in early pregnancy. [ABSTRACT FROM AUTHOR]

Objective: To evaluate whether hysteroscopic septoplasty should be performed in all women diagnosed with subseptate uterus.Methods: In a prospective study, 138 patients diagnosed with subseptate uterus at the First Affiliated Hospital of Guangxi Medical University, Nanning, China, were enrolled between January 1, 2006, and March 1, 2011, and reproductive outcomes were compared among women who did and those who did not undergo hysteroscopic resection. Women were divided in 2 groups: group A comprised women with a history of recurrent spontaneous abortion (RSA), and was subdivided into control (A1) and surgery (A2) groups; group B comprised women with no history of poor reproductive outcomes, and was subdivided into control (B1) and surgery (B2) groups.Results: The rates of pregnancy and term delivery were higher in group A2 than in group A1 (P<0.05). The incidence of RSA and preterm delivery was higher in group A1 than in group A2 (P<0.05). There was no difference in pregnancy rate, incidence of RSA, or preterm or term delivery between group B1 and group B2.Conclusion: Hysteroscopic septoplasty significantly improved pregnancy outcomes in women with a history of RSA, but did not influence reproductive outcomes in women with no history of poor pregnancy outcomes. [ABSTRACT FROM AUTHOR]

Problem: During normal pregnancy, delicate crosstalk is established between fetus‐derived trophoblasts and maternal immune cells to ensure maternal‐fetal tolerance and successful placentation. Dysfunction in these interactions has been highly linked to certain pregnancy complications. Method of study: Naïve CD4+T cells were cultivated with or without 1st trimester derived trophoblast cell line HTR8/SVneo cells in the absence or presence of T helper 17 (Th17) or regulatory (Treg)cell‐inducing differentiation conditions. After 5 days of co‐culture, HTR8/SVneo cells and CD4+T cells were harvested and analyzed using flow cytometry. Results: CD4+T cells exposed to HTR8/SVneo cells showed enhanced induction of CD4+Foxp3+Treg cells with strong expression of TGF‐β1 and inhibitory molecules (cytotoxic T lymphocyte‐associated protein‐4 [CTLA‐4], T‐cell immunoglobulin mucin‐3 [Tim‐3], and programmed cell death‐1 [PD‐1]). Though not effecting Th17 differentiation, exposure to HTR8/SVneo cells promoted increased expression of proliferative and apoptotic markers on Th17 cells. Co‐culture with Th0 cells, or differentiated Th17 or Treg cells, down‐regulated Caspase‐3 and MMP‐9 (but not MMP‐2) expression in HTR8/SVneo cells, while promoting Ki67 expression. Conclusions: HTR8/SVneo cells regulated maternal CD4+T‐cell differentiation, resulting in the expansion of immunosuppressive Treg cells, while CD4+T cells might promote the growth, and control the invasiveness of HTR8/SVneo cells. Thus, a bidirectional regulatory loop might exist between trophoblasts and maternal immune cell subsets, thereby promoting harmonious maternal‐fetal crosstalk. [ABSTRACT FROM AUTHOR]