Decidualization involves the proliferation and differentiation of fibroblast-like endometrial stromal cells into epithelioid-shaped and secretory ‘decidual’ cells in response to steroid hormones. Human decidual cells produce insulin-like growth factor-binding protein-1 and prolactin (PRL), two well-recognized markers of decidual cell maturation and a proteoglycan decorin (DCN). We reported that DCN restrains the human trophoblast renewal, migration, invasion and endovascular differentiation needed for uterine arterial remodeling during normal pregnancy. DCN overproduction by the decidua is associated with a hypo-invasive placenta and a serious pregnancy disorder, pre-eclampsia (PE). Furthermore, elevated maternal plasma DCN levels during the second trimester is a predictive biomarker of PE. While these paracrine roles of decidua-derived DCN on trophoblast physiology and pathology have been well-defined, it remains unknown whether DCN plays any autocrine role in decidual cell development. The objectives of this study were to examine: the kinetics of DCN production during decidualization of human endometrial stromal cells; gestational age-related changes in DCN production by the first trimester decidua; and a possible autocrine role of DCN on decidual cell maturation. We found that DCN production is enhanced during decidualization of both primary and immortalized human endometrial stromal cells in vitro and during early gestation in decidual samples tested ex vivo, and that it is important for endometrial stromal cell maturation into a decidual phenotype. Decorin-depleted human endometrial stromal cells exposed to decidualizing stimuli failed to mature fully, as evidenced by fibroblastoid morphology, reduced insulin-like growth factor-binding protein-1 and PRL expression, and reduction in cellular ploidy. We identified heart and neural crest derivatives-expressed protein 2, and progesterone receptor as potential downstream mediators of DCN effects.

中文翻译：

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人类蜕膜产生的核心蛋白聚糖：在蜕膜细胞成熟中的作用。

蜕膜化涉及成纤维细胞样子宫内膜基质细胞响应类固醇激素而增殖和分化为上皮样和分泌性“蜕膜”细胞。人类蜕膜细胞产生胰岛素样生长因子结合蛋白 1 和催乳素 (PRL)，这两种公认的蜕膜细胞成熟标志物和蛋白聚糖核心蛋白聚糖 (DCN)。我们报告说，DCN 抑制了正常妊娠期间子宫动脉重塑所需的人类滋养层更新、迁移、侵袭和血管内分化。蜕膜产生的 DCN 过量与低侵袭性胎盘和严重的妊娠疾病、先兆子痫 (PE) 相关。此外，孕中期升高的母体血浆 DCN 水平是 PE 的预测生物标志物。虽然蜕膜衍生的 DCN 在滋养层生理学和病理学上的这些旁分泌作用已经明确，但 DCN 是否在蜕膜细胞发育中发挥任何自分泌作用仍然未知。本研究的目的是检查：人子宫内膜基质细胞蜕膜化过程中 DCN 产生的动力学；孕早期蜕膜中 DCN 产生的与孕龄相关的变化；以及 DCN 对蜕膜细胞成熟的可能自分泌作用。我们发现在原代和永生化人子宫内膜基质细胞的蜕膜化过程中，DCN 的产生增加 人子宫内膜基质细胞蜕膜化过程中 DCN 产生的动力学；孕早期蜕膜中 DCN 产生的与孕龄相关的变化；以及 DCN 对蜕膜细胞成熟的可能自分泌作用。我们发现在原代和永生化人子宫内膜基质细胞的蜕膜化过程中，DCN 的产生增加 人子宫内膜基质细胞蜕膜化过程中 DCN 产生的动力学；孕早期蜕膜中 DCN 产生的与孕龄相关的变化；以及 DCN 对蜕膜细胞成熟的可能自分泌作用。我们发现在原代和永生化人子宫内膜基质细胞的蜕膜化过程中，DCN 的产生增加体外和蜕膜样品中妊娠早期测试离体，和这是子宫内膜间质细胞成熟重要成蜕膜表型。核心蛋白聚糖耗尽的暴露于未能充分成熟decidualizing刺激人子宫内膜基质细胞，如成纤维通过形态学证明，降低的胰岛素样生长因子结合蛋白-1和PRL表达，和减少在蜂窝倍性。我们将心脏和神经嵴衍生物表达的蛋白 2 和孕酮受体鉴定为 DCN 效应的潜在下游介质。