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Study function of endometrial mucin-2 on the tight junction structure of epithelial cells under bacterial endotoxins
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  • Chenchen Wu,
  • Dujian Yan,
  • Mengru Zhou,
  • Dezhang Lu
Chenchen Wu
Northwest A&F University College of Animal Science and Technology

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Dujian Yan
Shanghai Zhonghua College of Vocational Technology
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Mengru Zhou
Northwest A&F University College of Animal Science and Technology
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Dezhang Lu
Northwest A&F University College of Animal Science and Technology
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Abstract

To analysis fuction of mucin-2 on the tight junction structure of uterus under dacterial endotoxins. Endotoxins are produced by lipopolysaccharides (LPS) components in the outer membrane of gram-negative bacteria, which cause great harm to humans and animals. A vast number of mucin-2 (MUC2) forms a mucus layer covering endometrial epithelial cells. The mucus layer and tight junction structure of epithelial cells can resist damage from foreign bacteria and their toxins in the uterus. However, the interaction between MUC2 and tight junction proteins is not clear. In this experiment, we used endotoxin to treat uterine tissue pre- and postweaning in female mice and observed the effect of endotoxin-induced MUC2 on the tight junction structure of epithelial cells in the uterus. The results showed that a large amount of endotoxin accumulated in the uterus after 21 days of postdelivery weaning. The thicker mucus layer of the uterus is used to prevent the translocation of endotoxin at 21d postdelivery. When endotoxin acts on the uterus to thin its mucous layer, the cells in the lamina propria of the uterus secrete a large number of glycoprotein particles at 27d postdelivery. The glycoprotein particles are incompletely glycosylation-modified MUC2, which can interact with the cell membrane and are released in large quantities in the form of exocytosis. These glycoprotein particles can significantly repair tight junction structures in the intercellular space and significantly increase the expression of claudin-1, JAM, E-cadherin, ZO-1 and desmosome proteins after endotoxin treatment. The results of the present work showed that endotoxins can thin the uterine mucus layer and accelerate the release of incompletely glycosylated MUC2 from lamina propria cells. In intercellular spaces, MUC2 can increase its expression levels and distribution area to repair the tight junction structure of cells with larger gaps. Further strengthening of the barrier prevents endotoxin translocation by repairing the tight junction structure of uterine epithelial cells.