Progesterone induces the expression of lipocalin-2 through Akt-c-Myc pathway during mouse decidualization

Progesterone induces the expression of lipocalin-2 through Akt-c-Myc pathway during mouse decidualization
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黄体酮在小鼠蜕膜化过程中通过 Akt-c-Myc 通路诱导 lipocalin-2 的表达

DOI:
10.1002/1873-3468.12304
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发表时间:
2016-08-01
期刊:
影响因子:
3.5
通讯作者:
Liang, Xiao-Huan
Liang, Xiao-Huan
中科院分区:
生物学3区
文献类型:
--
作者:
Liu, Yue-Fang;Deng, Wen-Bo;Liang, Xiao-Huan

文献摘要

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脂质运载蛋白-2(Lipocalin-2,Lcn 2)是一种小分子糖蛋白,参与多种生物学过程,如炎症和抗菌反应。在我们的研究中,Lcn 2在妊娠第5天着床部位的腔下基质细胞中表达。Lcn 2在基质细胞中的表达受孕酮通过Akt-c-Myc信号通路的调控。来自Lcn 2敲低和重组蛋白处理的数据表明,Lcn 2促进基质细胞中mPGES-1的表达。Lcn 2和mPGES-1的表达被脂多糖(LPS)强烈刺激,表明Lcn 2介导LPS诱导的炎症。这些发现揭示了Lcn 2在蜕膜化过程中的作用。
Lipocalin-2 (Lcn2) is a small glycoprotein involved in a number of biological processes such as inflammation and antibacterial response. In our study, Lcn2 is expressed in the subluminal stromal cells at implantation site on day 5 of pregnancy. The expression of Lcn2 in stromal cells is under the control of progesterone through Akt-c-Myc signaling pathway. Data from Lcn2 knockdown and recombinant protein treatments indicate that Lcn2 promotes mPGES-1 expression in stromal cells. The expression of Lcn2 and mPGES-1 is strongly stimulated by lipopolysaccharide (LPS), indicating that Lcn2 mediates LPS-induced inflammation. These findings shed light on the role of Lcn2 during decidualization.