Abstrakt

The Up-Regulation of SOCS3 Expression by Estrogen Simulation in Macrophages is not Through the Estrogen Receptor (ER) Signaling

Yang Y*, Zhang T, Yuan Z and Xu D

Immuno-inflammation hypothesis is the hot spot of atherosclerosis mechanism at present, while SOCS (Suppresor of Cytokine Sigaling) is the key inhibitor of cytokine and its immuno-inflammatory signaling. Recent researches suggest that SOCS3 is probably a latent atherosclerosis protective factor, while estrogen is shown to play a protective role to atherosclerosis. In this paper, we demonstrated that estrogen could increase SOCS3 expression in a dose dependent manner in macrophages cells. We further demonstrated that estrogen up-regulate SOCS3 expression is not through the traditional ER (estrogen receptor) pathway as detected by estrogen inhibitor-ICI182780. Our findings illustrate more details about the mechanism of estrogen-induced atherosclerosis protection.