S100P regulates trophoblast-like cell proliferation via P38 MAPK pathway.

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. S100P最初从胎盘中分离，在滋养细胞中有非常高的表达水平，但是它在滋养细胞增殖过程中的作用还没有被研究过。我们这项研究的目的是研究S100P在人类胎盘发育过程中的潜在作用，以及对细胞功能的表达调控和与滋养样细胞相关的分子机制的影响。我们发现，早孕期流产的病人比正常的妊娠孕妇的S100P的表达水平显著下降。上调S100P在JAR细胞的表达，可以促进JAR细胞的增殖，并增加了磷酸化的P38促分裂原活化蛋白激酶和p-ERK蛋白激酶的表达。然而，S100P对JAR细胞增殖的效应可以被P38抑制剂SB203580阻断，但不被ERK抑制剂PD98059抑制。这些结果表明，S100P可能在正常妊娠发展中有一定的生理作用，通过调节P38 MAPK途径调节滋养样细胞增殖。 [ABSTRACT FROM PUBLISHER]