title: Inducers of G-protein coupled estrogen receptor (GPER) in endometriosis: potential implications for macrophages and follicle maturation.
abstract: Endometriosis is an estrogen dependent chronic inflammation and thus a condition of stress. Though the G-protein coupled estrogen receptor (GPER) has been shown to be up-regulated in ovarian endometriosis, insights involved in inducing this receptor expression are largely elusive. Therefore, this study investigated whether stress-related factors (ACTH, prednisolone) or inflammatory factors (IL-1β, TNFα, and PGE(2)) factors may affect GPER. To further link GPER to endometriosis pathophysiology it was tracked in macrophages and follicles of endometriotic ovaries. This study found GPER expression to be modulated by stress-related hormones as well as inflammation and to be up-regulated in endometriosis-associated macrophages. At the same time, follicles of ovaries affected by endometriosis presented significantly reduced GPER positivity when compared to controls, suggesting a possible way by which endometriosis may affect folliculogenesis. The multiple roles of GPER as presented herein make it a promising future candidate for targeted molecular endometriosis treatment.
authors: Department of Obstetrics and Gynaecology, Campus Innenstadt, Ludwig-Maximilians-University of Munich, Munich, Germany. Sabine.Heublein@med.uni-muenchen.de
authors: Sabine
authors: S
authors: Heublein
authors: Thomas
authors: T
authors: Vrekoussis
authors: Christina
authors: C
authors: Kuhn
authors: Klaus
authors: K
authors: Friese
authors: Antonis
authors: A
authors: Makrigiannakis
authors: Doris
authors: D
authors: Mayr
authors: Miriam
authors: M
authors: Lenhard
authors: Udo
authors: U
authors: Jeschke
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000276:immunology / Q000378:metabolism; D000328:Adult; D045744:Cell Line, Tumor; D015232:Dinoprostone / Q000276:immunology / Q000378:metabolism; D004715:Endometriosis / Q000188:drug therapy / Q000378:metabolism*; D004717:Endometrium / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism*; D053583:Interleukin-1beta / Q000276:immunology / Q000378:metabolism; D008875:Middle Aged; D058990:Molecular Targeted Therapy; D011239:Prednisolone / Q000276:immunology / Q000378:metabolism; D011960:Receptors, Estrogen / Q000235:genetics / Q000378:metabolism*; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism*; D013315:Stress, Psychological / Q000188:drug therapy / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism; D055815:Young Adult
chemical_list: C109584:GPER1 protein, human; D053583:Interleukin-1beta; D011960:Receptors, Estrogen; D043562:Receptors, G-Protein-Coupled; D014409:Tumor Necrosis Factor-alpha; D000324:Adrenocorticotropic Hormone; D011239:Prednisolone; D015232:Dinoprostone