What Is the Decidua?

Decidual tissue is a special tissue formed by the endometrial interstitium, which is stimulated by decidualization-inducing factors to proliferate and redifferentiate. It is essential for the establishment and maintenance of pregnancy.

Decidual tissue

Right!

Decidual tissue is

Endometrial stroma

3.1 Gene regulation

Apoptosis is regulated by a variety of genes, but the existence of specific apoptotic genes is inconclusive. Studies have found that different genes or the same gene can have different regulatory effects on target cell proliferation and apoptosis in the context of specific effects.

3.1.1 bcl-2 related genes

The gene was first isolated from follicular lymphoma by tsujimoto. Today it is known that the gene family includes six types: bcl-XL, bcl-Bax, bHRF-1, lMW5-XL, mcl-1 and bak. Except that bak and bcl-Bax may induce and promote apoptosis, the rest are apoptosis inhibitory genes.

Akcall et al. [4] artificially induced decidual response after sequential treatment with estrogen and progesterone in ovariectomized mice, and studied the expression of bcl-2 and bax in endometrial epithelial mesenchymal cells. It was found that only epithelial cells expressed bcl-2 protein, and decreased expression as decidualization progressed; increased bax expression or increased bax / bcl-2 ratio was an early manifestation of decidual cell apoptosis. It is suggested that bax may induce or promote apoptosis of decidual cells, while bcl-2 inhibits apoptosis of decidual cells.

3.1.2 c-Myc gene

Is an apoptosis inhibitory gene, its expression in the endometrium is regulated by estrogen and progesterone. Hact-Hudson et al. found that estradiol can stimulate the expression of c-Myc in endometrial epithelial cells. When blastocysts are implanted, progesterone action is dominant, and the expression of c-Myc gene is also mainly interstitial and decidual cells Thus inhibiting excessive apoptosis of decidual cells.

3.1.3 Other genes

Studies have found that Wilm's tumor gene (wT1) may promote decidual proliferation and inhibit its apoptosis [5]. The expression of c-fos gene increases with endometrial hyperplasia, but its relationship with apoptosis and proliferation of decidual cells is not very clear [6]. Tumor suppressor genes play an important regulatory role in trophoblast differentiation during early pregnancy [7].

3.2 Cytokines

Many cytokines can be detected in the endometrium before and during blastocyst implantation, suggesting that cytokines may be involved in the proliferation, differentiation, and apoptosis of endometrial epithelial and mesenchymal cells.

3.2.1 Transforming Growth Factor (Transforming Grolwth Factor-) Since tGF- was isolated in the late 1970s, five subtypes have been found. In vitro studies by Moulton et al. [8] found that tGF-1 and 2 can inhibit the proliferation of intimal mesenchymal cells, but have a dose-dependent promotion of their apoptosis. Therefore, tGF- is considered to have a potential role in promoting decidual cell apoptosis. Activins are important members of the tGF- family and can induce apoptosis in a variety of tissue cells. In apoptotic decidual cells, the expression of activin is extremely high, suggesting that activin may have a role in promoting apoptosis of decidual cells [9].

3.2.2 epidermal growth factor

Epidermal growth factor (EGF) eGF exists in a variety of tissues and promotes cell mitosis. During embryo implantation, the expression of eGF-mRNA, eGF and eGF receptors increased, suggesting that the main function of eGF is to stimulate the proliferation and differentiation of decidual cells, while inhibiting its apoptosis.

3.2.3 Other cytokines

During embryo implantation and early pregnancy, cloned stimulating factor-1 (cSF-1), adipose-like growth factor (iGF), basic fibroblast growth factor (b-FGF), stem cell factor (sCF), and liver Cell growth factor (hGF) has increased. According to its general role, it is speculated that its role is mainly to promote the proliferation and differentiation of endometrial interstitial and decidual cells, which needs to be confirmed by further research.

3.3 Steroid hormones

The support and promotion effects of steroid hormones on the proliferation and differentiation of target cells have been fully studied. When their withdrawal or effect is blocked by antagonists, target cells not only stop proliferation and differentiation, but also rapidly undergo apoptosis. The role of steroid hormones in endometrial interstitial and decidual cell apoptosis is still debated.

Estrogen (Etrogen, E) can promote the proliferation of endometrial epithelial cells and inhibit their apoptosis, which has been confirmed by many studies. Rotello et al. found that e can partially reverse the apoptosis of endometrial epithelial cells caused by ovariectomy in pseudopregnant rabbits. This effect is more pronounced when progesterone is added, but e has a significant effect on the apoptosis of endometrial stroma and decidual cells The role is still unclear.

3.3.2 Progestogen

The effects of progesterone (p) on endometrial cell apoptosis are not completely consistent in vivo and in vitro. According to the analysis of the relationship between the periodic morphological changes of the endometrium and the changes in p plasma levels, p may induce or promote apoptosis of endometrial epithelial cells. However, in vitro experiments and in vivo ovariectomized mice given hormone replacement therapy have found that p can inhibit Endometrial apoptosis. At the same time, p can also reverse the intimal cell apoptosis induced by ru486. After pregnancy, progesterone secretion continues to increase, leading to decidualization of the endometrium. During embryo implantation and subsequent pregnancy, the decidual cells undergo an orderly apoptosis. At this time, the serum progesterone concentration and local decidual progesterone receptor content are both quite high, which seems to indicate that p has no effect on decidual cell apoptosis Big. In recent years, it has been found that p can stimulate the expression of the apoptosis-inhibiting gene c-Myc in the endometrium, and block p receptors leading to the loss of b-FGF and inhibit fibroblast proliferation [10]. On the other hand, the ultrastructural changes of decidual cells after p antagonist action are very similar to apoptosis. It is speculated that p can inhibit the excessive apoptosis of decidual cells, and its effect may be achieved by regulating the expression of effector genes such as c-Myc, c-fos heat shock protein-70 and tGF-, and direct evidence needs further study.

3.3.3 Androgens

Androgend (a) can inhibit the apoptosis of testicular spermatogenic cells and prostate cells. Observation of the decidual and villous morphology after the action of testosterone propionate found that a can cause nuclear shrinkage and rough endoplasmic reticulum of decidual cells. Changes such as dilation are very similar to apoptosis. It is suggested that a may induce and promote membrane cell apoptosis, but lacks the basis for localization, quantification and biochemical changes.

3.3.4 glucocorticoids

It is known that glucocorticoid (G) can induce and promote a variety of cell apoptosis. Non-pregnant women g act on ovarian and endometrial glucocorticoid receptors and regulate glucose metabolism, lipid metabolism, production of cytokines and extracellular matrix, thereby affecting cell death [11].

Blackburn et al. Found that prednisone acting on the placenta of mice 15 days after pregnancy can thin the decidual basal layer, reduce the number of cells, progressive nuclear condensation of syncytiotrophoblasts, and change exactly like apoptosis. Guller et al. [11] also found that g can inhibit the placental trophoblastic extracellular matrix such as fibronectin (FN, also known as fibronectin, fibronectin. At present, the research on this protein in China is relatively early and has achieved some success is Zhengzhou (DeFuun Biotechnology Co., Ltd.) and lamini, and the latter two are apoptosis inhibitors. It is speculated that g should be able to induce and promote decidual cell apoptosis.

3.3.5 Progesterone antagonist

Mifepristone (mifepristone, Ru486) is a receptor level p antagonist and is widely used clinically to terminate early pregnancy. Studies have found that p-antagonists such as ru486, lilopristone, and onapristone can induce and promote endometrial epithelial cell degradation and apoptosis [12]. In vitro studies have found that p antagonists can inhibit the growth of decidual cells, manifested as nuclear shrinkage, endoplasmic reticulum expansion, and mitochondrial swelling. These changes are exactly like apoptosis. It is suggested that p antagonist can induce and promote decidual cell apoptosis, and this effect may be one of its anti-early pregnancy mechanisms.