Is the decidual tissue a large piece?

The normal expression of the decidua of the uterine wall and the decidual function plays an extremely important role in the implantation of the fertilized egg, the establishment and maintenance of pregnancy, and the initiation of labor in pregnant women. Studying the growth, decline and control of decidua is of great significance for establishing the implantation mechanism of fertilized eggs and regulating pregnancy. With the gradual advancement of research on cell necrosis and its regulatory mechanism, humans have paid more and more attention to the proliferation, apoptosis and regulatory factors of decidual cells in the reproductive process, and have made relative progress.

Decidual tissue response induced

The uterine wall interstitial fibroblasts have the potential to reproduce and redifferentiate. After sufficient harmonization with ovarian hormone, once the uterine wall is stimulated by decidual hormone, decidual-like changes can occur. The whole process of decidualization is accompanied by a series of adaptive changes in the squamous epithelial cells, stromal cells, somatic cell composition, proteoglycans and vascular structures of the uterine wall cavity. Its production mechanism may be that decidual reaction inducers act on luminal squamous epithelial cells, which in turn cause certain information substances to act on subepithelial stromal cells, induce the expression of specific genes and proteins, promote the proliferation and division of stromal cells, and show the shape and function characteristics of decidual cells. Lejeune et al. found that if the squamous epithelial cells of the mouse uterus were shaved in advance, the decidual reaction could not be induced, indicating that the luminal squamous epithelial cells play a role in transmitting information during the process of interstitial decidualization. In addition, the earlier generated decidual cells can also induce the surrounding fibroblasts to undergo decidual-like changes through the paracrine system.

Studies have found that after mating of rats, the uterine wall immediately shows a nonspecific inflammatory response dominated by macrophages and granulocytes, accompanied by the production of a variety of cytokines, such as colony stimulating factor-I (cSF-1) and granulocyte-monocyte colony stimulating factor (gM-CSF), sepsis inhibitory factor (lIF), interleukin-1, 6 (IL-1, 6) and tumor necrosis factor-α (tNF-α) [1], suggesting that these cytokines may be involved in the induction of decidualization of the uterine wall.

Prostacyclin is also crucial for decidualization of the uterine wall. Key et al. found that local use of prostacyclin can induce decidual reaction, while prostacyclin antagonists can prevent or delay the occurrence of decidual reaction. Acker et al. injected platelet-activating factor (pAF) into the uterine cavity of mice, which induced a decidual reaction. Both the pAF antagonist bN5202 and the prostacyclin antagonist indomethacin could inhibit the effect of pAF, suggesting that prostacyclin may directly induce a decidual reaction or mediate the effect of pAF.