ERp29 affects the migratory and invasive ability of human extravillous trophoblast HTR-8/SVneo cells via modulating the epithelial-mesenchymal transition.

Dysfunction of trophoblast metastasis into the endometrium is the main cause of pre-eclampsia (PE); however, the factors affecting this process are still unclear. In this study, we found that endoplasmic reticulum protein 29 (ERp29), one molecular chaperone of the endoplasmic reticulum, was aberrantly upregulated in the placenta of pre-eclamptic patients compared with healthy controls. Then, an in vitro study using human extravillous trophoblast HTR-8/SVneo cells showed that ERp29 upregulation could inhibit the migratory and invasive ability of HTR-8/SVneo cells, while ERp29 downregulation had the opposite effect. Mechanical experiments confirmed that ERp29 blocked trophoblast metastasis via inhibiting the process of epithelial-mesenchymal transition and affecting the Wnt/ß-catenin signaling pathway. In conclusion, this study revealed the important role of ERp29 in trophoblast metastasis and improved the mechanical understanding of PE occurrence.

A multifactorial analysis of the pregnancy outcomes in cytomegalovirus-infected women.

AIMS: To investigate the impacts of cytomegalovirus (CMV) viral load, TORCH (toxoplasmosis, others, rubella, CMV and herpes) coinfections, CMV glycoprotein B (gB) genotypes and maternal genetic polymorphisms on pregnancy outcomes among CMV-infected women. METHODS: A total of 731 CMV-infected pregnant women (634 and 97 with normal and adverse pregnancy outcomes, respectively) were recruited. CMV load quantification and screening of TORCH coinfections were performed by using real-time polymerase chain reaction (PCR) and immunodetection techniques, respectively. Genotyping of CMV gB and maternal NFKB1 -94 ins/del, NFKBIA -826C/T and -881A/G polymorphisms was performed by using PCR-restriction fragment length polymorphism. RESULTS: We found that the mean CMV viral load in women with adverse pregnancy outcomes was significantly higher than that in women with normal outcomes at all pregnancy stages (p < 0.01). We also found that TORCH coinfections resulted in a 1.65-fold (95% CI = 1.00-2.73) increase in the risk of adverse pregnancy outcomes (p = 0.05). Additionally, we noticed no significant difference in the distribution of CMV gB genotypes between women with normal and adverse pregnancy outcomes (p = 0.42). We also observed that the ins/ins variant genotype of the NFKB1 polymorphism could reduce the risk of adverse pregnancy outcomes (OR = 0.38, 95% CI = 0.15-0.98; p = 0.04). CONCLUSION: CMV viral load, TORCH coinfections and maternal NFKB1 polymorphism could influence pregnancy outcomes among CMV-infected women.