The relationship between the placenta and the fetus is also regulated by the immune system. These pathological changes can affect the exchange of substances and gases between the mother and fetus, which might be the cause of adverse pregnancy outcomes, such as stillbirth. The gap between the villi was narrow, with the evidence of chronic inflammation. In our early clinical studies, it was found that the local villi of placental specimens from DIP women were immature, showing signs of edema and degeneration. In DIP, changes in placental morphology and histology may result in functional changes. This might be caused by the release of vascular endothelial growth factor and fibroblast growth factor from the placenta. A previous study has reported an increased placenta–fetal weight ratio with a rising placental volume and weight due to poor blood glucose control in women with DIP. In women with diabetes in pregnancy (DIP), the trophoblast cells may undergo a series of pathological changes in response to different blood glucose environments. The function of trophoblast cells can be affected by maternal blood glucose fluctuations, with various subsequent pathophysiological outcomes.
The latter are in direct contact with the maternal blood during pregnancy. Embryonic tissues mainly include fetal blood vessels and trophoblast cells. The placenta contains both maternal and embryonic tissues. Furthermore, the proliferation of trophoblasts was not affected by the osmotic pressure. A high-glucose environment inhibited initial cell proliferation, which could be moderately restored after self-regulation. In summary, the blood glucose concentration might influence the proliferation of trophoblast cells. Compared with 24 h, cell proliferative activity was restored to a certain extent after 48 h in the high-glucose group. The proportion of cells in the G2/M phase was higher in the low-glucose group than in the other groups, and it was lower in the G1 phase and higher in the S phase in the high-glucose group than in the other groups. The cell number was relatively decreased and morphological changes were intermediate in the high-glucose group compared with the low-glucose groups.
The cell cycle and apoptosis were examined by flow cytometry. The cell morphology and proliferation were determined by microscopy and a cell counting kit-8 assay. In addition, the cells were treated with 5 mmol/L glucose (normal) and 5 mmol/L glucose + 20 mmol/L mannitol (mannitol).
HTR8/SVneo cells were treated with 0 (no glucose), 1 (low glucose), 5 (normal), and 25 mmol/L (high glucose) glucose. This study investigated the effects of glucose and osmotic pressure on the proliferation and cell cycle of trophoblast cells.
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