Estrogen Receptors in Leukocytes - Possible Impact on Inflammatory Processes in the Female Reproductive System

Estrogens carry out various reproductive and non-reproductive functions. Traditionally, estrogen action was thought to be solely mediated through its nuclear receptors estrogen receptor (ER)┙ and ER┚ (Deroo & Korach, 2006). However, recently a membrane bound G protein-coupled receptor-30, now designated as G protein-coupled estrogen receptor1(GPER), has been described as a receptor for estrogen (Prossnitz et al., 2007). ER┙ and ER┚ belong to the nuclear receptor superfamily and functions as ligand activated transcriptional factors. The classical mechanism of nuclear ER action involves ligand binding to receptors, dimerization and binding to specific response elements of the target genes to elicit a transcriptional response. Although estrogen action is mostly targeted towards reproductive tissues, they also act via ERs in non-reproductive target tissues (Diel, 2002; Manolagas & Kousteni, 2001; Walker & Korach, 2004). Estrogens can also act rapidly through nongenomic mechanisms by binding to membrane bound ERs (Deroo & Korach, 2006; Prossnitz et al., 2007). GPER is a member of the G protein-coupled receptor superfamily containing seven transmembrane helices and mediates estrogen-dependent kinase activation as well as transcriptional responses (Prossnitz et al., 2007). Receptors for estrogens are present in leukocytes and perform various functions. ERs and several of their splice variants have been identified in polymorphonuclear and mononuclear leukocytes isolated from peripheral blood of both men and women (Stygar et al., 2006). ERs are present in a variety of leukocytes like myeloid progenitor cells, neutrophils, lymphocytes, natural killer cells, macrophages, monocytes, mast cells etc. This chapter will summarize the publications on the role of estrogen in leukocytes and its implications in female reproduction.