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首页> 外文期刊>American Journal of Physiology >cGMP-dependent protein kinase II determines (3-catenin accumulation that is essential for uterine decidualization in mice
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cGMP-dependent protein kinase II determines (3-catenin accumulation that is essential for uterine decidualization in mice

机译：CGMP依赖性蛋白激酶II确定（3-连环蛋白积累，对小鼠的子宫蜕皮病至关重要

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In the early phase of pregnancy, decidualization is an indispensable event after mammal embryo implantation, accompanied by proliferation and differentiation of uterine stromal cells. Type II cGMP-dependent protein kinase (Prkg2) belongs to the family of serine/threonine kinase, which plays multiple roles in cellular signaling pathways to control proliferation and differentiation. However, the regulatory function and molecular mechanism of Prkg2 in decidualization are still unknown. In this study, we show that Prkg2 has a gradually increased expression pattern during peri-implantation and artificial decidualization, and the expression of Prkg2 is induced by estrogen and progesterone in the ovariectomized mouse uteri and primary cultured uterine stromal cells, the process of which is blocked by treating with estrogen receptor (ER) antagonist (ICI-182,780) and progesterone receptor (PR) antagonist (RU-486). Inhibition of Prkg2 activity by HA-100 promotes uterine stromal cell proliferation but compromises decidualization with decreased expression of prolactin family 8, subfamily a, member 2. In addition, the functional regulation of decidualization by Prkg2 is accomplished by its induced phosphorylation of glycogen synthase kinase-3beta (GSK-3beta) at serine-9, which results in accumulation of beta-catenin in the decidual cells. Taken together, our findings demonstrate that estrogen and progesterone upregulate the expression of Prkg2 in uterine stromal cells depending on ER and PR; Prkg2 promotes phosphorylation of GSK-3beta at serine-9 and inactivates it, leading to the accumulation of p-catenin and promoting the process of decidualization. In addition to revealing the regulatory mechanism of Prkg2 that ensures the success of uterine decidualization, our findings will contribute to the understanding in the maintenance of early pregnancy.
机译：在妊娠早期阶段，DeCiAnization是哺乳动物胚胎植入后的不可或缺的事件，伴有子宫基质细胞的增殖和分化。 II型CGMP依赖性蛋白激酶（PRKG2）属于丝氨酸/苏氨酸激酶系列，其在细胞信号传导途径中起多种作用以控制增殖和分化。然而，PRKG2在DeCiAnization中的调节功能和分子机制仍然未知。在这项研究中，我们表明，PRKG2在植入过程中具有逐渐增加的表达模式，并且在卵巢切除小鼠子宫和初级培养的子宫基质细胞中通过雌激素和孕酮诱导PRKG2的表达，其方法是通过用雌激素受体（ER）拮抗剂（ICI-182,780）和孕酮受体（PR）拮抗剂（RU-486）来阻止。通过HA-100抑制PRKG2活性促进子宫基质细胞增殖，但损害了催乳素家族8，亚家族A，构件2的表达降低的蜕皮化。此外，PRKG2的蜕皮化的功能调节是通过其诱导糖原合酶激酶的磷酸化完成的丝氨酸-9的-3beta（GSK-3beta）导致蜕膜细胞中β-连环蛋白的积累。我们的研究结果一起证明了雌激素和孕酮上调了子宫基质细胞中Prkg2的表达，这取决于ER和Pr; Prkg2在丝氨酸-9促进GSK-3β的磷酸化并使其失活，导致p-catenin积累并促进蜕膜化的过程。除了揭示PRKG2的监管机制，确保子宫蜕膜化成功，我们的调查结果将有助于在妊娠早期的维持中的理解。

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