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Erin Greaves

Technical Summary

The etiology of endometriosis remains unknown and its presentation is extremely heterogeneous. Our research focuses on the role of macrophages in endometriosis. Macrophages are present in high numbers in lesions and within the pelvic cavity of patients with endometriosis. They play a critical role in the growth and vascularization of endometriosis lesions. We have recently demonstrated a reciprocal interaction between macrophages and nerves fibres that contributes to innervation of lesions, sensitization of nerve fibres and pain in the disorder. Currently we are beginning to investigate the origin and phenotypic heterogeneity of macrophages in endometriosis using lineage tracing, fate mapping and single cell discovery. Ultimately, we hope to know enough about disease-modified macrophages in endometriosis to successfully target populations of pathogenic macrophages and treat the symptoms of endometriosis.

Selected publications:

Greaves E, Horne AW,Jerina H, Mikolajczak M, Hilferty L, Mitchell R, Fleetwood-Walker SM, Saunders PT. EP2 receptor antagonism reduces peripheral and central hyperalgesia in a preclinical mouse model of endometriosis. Scientific Reports 7, 44169 (2017)

Greaves E, Temp J, Esnal-Zufiurre A, Mechsner S, Horne AW, Saunders PT. Estradiol Is a Critical Mediator of Macrophage-Nerve Cross Talk in Peritoneal Endometriosis. Am J Pathol 185,2286-97 (2015)

Greaves E, Grieve K, Horne AW, Saunders PT. Elevated peritoneal expression and estrogen regulation of nociceptive ion channels in endometriosis. J Clin Endocrinol Metab, 99, 1738-43 (2014)

Greaves E, Cousins FL, Murray A, Esnal-Zufiaurre A, assbender A, Horne AW, Saunders PT. A novel mouse model of endometriosis mimics human phenotype and reveals insights into the inflammatory contribution of shed endometrium. Am J Pathol 184, 1930-1939 (2014)

Greaves E, Collins F, Esnal A, Giakoumelou S, Horne AW, Saunders PT. Estrogen receptor (ER) agonists differentially regulate neuroangiogenesis in peritoneal endometriosis via the repellent factor SLIT3. Endocrinology, 155, 4015-26 (2014).