Mechanism of endometrial MUC2 in reproductive performance in mice through PI3K/AKT signaling pathway after lipopolysaccharide treatment

The objective of this study was to investigate the effects of exposure to endotoxin on the reproductive performance of humans and animals in pregnancy and delivery period. Mucin is considered to play a critical role in protecting the tissue epithelium. At pregnancy period, the MUC2 expression of uterus in the High LPS group was significantly higher than that in the Control group. The glycosaminoglycans of gland cells were secreted into the uterine cavity to protect the uterus. Then, the MUC2 layer became thinner, and LPS entered the lamina propria of the uterus. The mRNA expression of tight junction proteins showed a marked drop, and morphological damage of the uterus occurred. Subsequently, the glycosaminoglycans of gland cells in the High LPS and Low LPS groups increased with the increasing LPS dose, and the damage to the endometrial epithelium was repaired in female mice at Day 5 postdelivery. A low dose of LPS activated the PI3K/AKT signaling pathways to increase the glycosaminoglycans particles, while a high dose of LPS inhibited the PI3K/AKT signaling pathway to decrease the glycosaminoglycans particles. Taken together, our results suggest that gland cells secreted glycosaminoglycans particles into the uterine cavity by exocytosis to increase the thickness of the mucus layer to protect the uterus and that this process was regulated by PI3K/AKT signaling pathways.

Automated summary

This study investigated the effects of endotoxin exposure on the reproductive performance of humans and animals during pregnancy and delivery. The results showed that gland cells secreted glycosaminoglycan particles into the uterine cavity to increase the thickness of the mucus layer and protect the uterus. This process was found to be regulated by the PI3K/AKT signaling pathway.