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Progesterone induces the expression of lipocalin‐2 through Akt‐c‐Myc pathway during mouse decidualization
Author(s) -
Liu YueFang,
Deng WenBo,
Li ShuYun,
Yao MeiNan,
Liu Jie,
Dou HaiTin,
Zhao MengLong,
Yang ZengMing,
Liang XiaoHuan
Publication year - 2016
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12304
Subject(s) - decidualization , stromal cell , lipocalin , gene knockdown , inflammation , lipopolysaccharide , pi3k/akt/mtor pathway , protein kinase b , biology , endocrinology , microbiology and biotechnology , medicine , signal transduction , cancer research , chemistry , cell culture , immunology , genetics
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.