Erin Greaves

Dr Erin Greaves, Associate Professor

Following a PhD in developmental biology at the University of Leeds, I completed postdoctoral training at the (then) Medical Research Council (MRC) Human Reproductive Sciences Unit, University of Edinburgh with Philippa Saunders. In 2015, I established my lab at the MRC Centre for Reproductive Health, University of Edinburgh with an MRC Career Development Award Fellowship. In 2019, I moved to the University of Warwick as Assistant Professor.

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Team: Dr Matt Rosser (Lab manager), Dr Antonia Cuff (Postdoc), Priya Dhami (PhD student; ARAP), Niky Moolchandani-Adwani (PhD student; MRC-DTP), Eleanor Harrison (PhD Student; MRC-DTP), Iona McIntrye (PhD student; iCASE MRC-DTP).

Plain English

Endometriosis is the growth of uterine lining (endometrium) outside the uterus, usually within the pelvic cavity as ‘endometriosis lesions’. It is a common, chronic disorder affecting around 10% of reproductive age women and can cause chronic debilitating pelvic pain and infertility. Despite being such a common disorder with significant impacts on health related quality of life, there are very limited treatments available. In the lab we use a combination of patient biopsies, in vitro cell models and a mouse model of endometriosis in order to unravel mechanisms of disease and find potential therapeutic targets for this complex disorder.

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Erin Greaves

Dr Erin Greaves, Associate Professor

Email: Erin.Greaves@warwick.ac.uk

Google Scholar | ORCID

Plain English

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:

1. Forster R, Sarginson A, Velcikova A, Hogg C, Dorning A, Horne AW, Saunders PTK, Greaves E. Macrophages-derived insulin-like growth factor-1 is a key neurotrophic and nerve-sensitizing factor in pain associated with endometriosis. FASEB J, 2019 Oct;33(10):11210-11222.

2. 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)

3. 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)

4. 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)

5. 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)

6. 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).