Yu Hai-Fan, Yue Zhan-Peng, Wang Kai, Yang Zhan-Qing, Zhang Hong-Liang, Geng Shuang, Guo Bin
College of Veterinary MedicineJilin University, Changchun, People's Republic of China.
College of Veterinary MedicineJilin University, Changchun, People's Republic of China
J Endocrinol. 2017 May;233(2):145-157. doi: 10.1530/JOE-16-0583. Epub 2017 Feb 20.
Although has been proved to play an important role in uterine decidualization, its regulatory mechanism remains largely unknown. Here, we showed that was highly expressed in the decidual cells and promoted the proliferation of uterine stromal cells and expression of and , which were two well-known differentiation markers for decidualization. Further analysis revealed that might act downstream of and cAMP to regulate the differentiation of uterine stromal cells. Administration of cAMP analog 8-Br-cAMP to siRNA-transfected stromal cells resulted in an obvious increase of expression, whereas PKA inhibitor H89 impeded the induction of elicited by overexpression, indicating that cAMP-PKA signal mediates the regulation of on expression. In uterine stromal cells, knockdown of blocked the cAMP induction of Moreover, siRNA-mediated downregulation of impaired the stimulatory effects of overexpression on the expression of and , whereas constitutive expression of reversed the inhibitory effects of siRNA on stromal differentiation. Meanwhile, might play a vital role in the crosstalk between and Collectively, may act downstream of cAMP-PKA signal to mediate the effects of on the differentiation of uterine stromal cells through targeting .
尽管已被证明在子宫蜕膜化中起重要作用,但其调控机制仍 largely 未知。在此,我们表明其在蜕膜细胞中高表达,并促进子宫基质细胞的增殖以及两个著名的蜕膜化分化标志物的表达。进一步分析显示,其可能作用于[未提及的某个因子]和 cAMP 的下游来调节子宫基质细胞的分化。将 cAMP 类似物 8-Br-cAMP 给予转染了[未提及的某个因子] siRNA 的基质细胞导致[未提及的某个蛋白]表达明显增加,而 PKA 抑制剂 H89 阻碍了由[未提及的某个因子]过表达引发的[未提及的某个蛋白]的诱导,表明 cAMP-PKA 信号介导了[未提及的某个因子]对[未提及的某个蛋白]表达的调控。在子宫基质细胞中,敲低[未提及的某个因子]阻断了 cAMP 对[未提及的某个蛋白]的诱导。此外,siRNA 介导的[未提及的某个因子]下调削弱了[未提及的某个因子]过表达对[未提及的某个蛋白]和[未提及的某个蛋白]表达的刺激作用,而[未提及的某个蛋白]的组成型表达逆转了[未提及的某个因子] siRNA 对基质分化的抑制作用。同时,[未提及的某个因子]可能在[未提及的两个因子]之间的串扰中起关键作用。总体而言,[未提及的某个因子]可能作用于 cAMP-PKA 信号的下游,通过靶向[未提及的某个蛋白]介导[未提及的某个因子]对子宫基质细胞分化的影响。