Estrogen promotes SLE serum-induced skin inflammation via the estrogen membrane receptor GPER1

Skin injury is the second most common clinical manifestation in patients with systemic lupus erythematosus (SLE). Estrogen may affect the onset and development of SLE. In this study, we investigated the role of estrogen and its membrane receptor GPER1 in SLE-related skin injury in mice treated with...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of immunology (1950) 2017-05, Vol.198 (1_Supplement), p.55-55.1
Main Authors: Deng, Guo-Min, Cai, Zhenming, Xie, Changhao, Guo, Xuanxuan, Liu, Huicheng, Li, Xiaoyan, Fang, Xiang, Fei, Xibin, Guo, Yacong, Xu, Guangqiong, Dou, Hui
Format: Article
Language:English
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Skin injury is the second most common clinical manifestation in patients with systemic lupus erythematosus (SLE). Estrogen may affect the onset and development of SLE. In this study, we investigated the role of estrogen and its membrane receptor GPER1 in SLE-related skin injury in mice treated with SLE serum in vivo, and monocytes from mouse spleen in vitro. We found that skin injury induced by SLE serum was more severe in female mice and required monocytes. Estrogen promoted these effects through the membrane receptor GPER1 located in lipid rafts and that inhibition of lipid rafts and GPER1 suppressed SLE serum-induced skin inflammation and expression of inflammatory molecules. From these studies, we conclude that estrogen promotes the development of skin injury induced by SLE serum through the membrane receptor GPER1 and that lipid rafts play an important role in the regulatory effect of GPER1 in SLE skin inflammation.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.198.Supp.55.1