S100P regulates trophoblast-like cell proliferation via P38 MAPK pathway. (3rd October 2015)

• Record Type: Journal Article
• Authors: Zhu, Hai-Yan; Wang, Jun-Xia; Tong, Xiao-Mei; Xue, Ya-Mei; Zhang, Song-Ying
• Is Part Of: Gynecological endocrinology. Volume 31:Number 10(2015:Oct.)
• Page Start: 796
• Page End: 800
• Publication Date: 2015-10-03
• Subjects: Proliferation -- S100P -- trophoblast cell; Endocrine gynecology -- Periodicals; Generative organs, Female -- Diseases -- Periodicals; 618.1
• DOI: 10.3109/09513590.2015.1069268
• Languages: English
• ISSNs: 0951-3590

Abstract

Abstract: S100P was originally isolated from the placenta, and is expressed in very high levels in trophoblast cells, but its role on trophoblast cells proliferation has not yet been studied. In this study, we aimed to investigate the potential role of S100P in human placental development, and the impact of its expression regulation on cellular function as well as molecular mechanisms involved in trophoblast-like cells. We found that the expression of S100P in first trimester placenta was significantly reduced in spontaneous abortion patients with respect to normal pregnant women. Up-regulation of S100P in JAR cells promoted JAR cells proliferation, and increased the expression of phosphorylated P38 (p-P38) mitogen-activated protein kinase (MAPK) and p-ERK MAPK. However, the effects of S100P on JAR cells proliferation were prevented by P38 inhibitor-SB203580, but not by ERK inhibitor-PD98059. These results showed that S100P may have a physiological role in normal pregnant development, and regulate trophoblast-like cell proliferation via modulating the P38 MAPK pathway.