MRC Centre for Reproductive Health
MRC Logo JAN 2019

Dr Erin Greaves

Research interests and grants.

Dr Erin Greaves

MRC Career Development Research Fellow

Address

Street

The Queen’s Medical Research Institute
Edinburgh BioQuarter
47 Little France Crescent

City
Edinburgh
Post Code
EH16 4TJ

Biographical Information

In 2006 Erin graduated from Bradford University with a 1st class (hons) degree in Biomedical Sciences and went on to do a PhD at the University of Leeds in Developmental Biology. She defended her thesis in 2009 and began her postdoctoral training with Prof Philippa Saunders at the (then) MRC Human Reproductive Sciences Unit at the University of Edinburgh, working on endometrial function and endometriosis. In late 2014, she was awarded a prestigious MRC Career Development Award to start her own lab investigating the role of macrophages in endometriosis and endometriosis-associated pain at the MRC Centre for Reproductive Health. Recently, she was recognized with ‘Best New Investigator’ at the 62nd SRI Annual Meeting and won the David Healy Award at the 13th World Congress on Endometriosis. She has an active role on the CRH Postgraduate Committee as well as the Public Engagement and Communications Committee and is Associate Editor for Molecular Human Reproduction.

Selected Publications

1. 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).
2. Greaves E, Critchley HO, Horne AW, Saunders PT. Relevant human tissue resources and laboratory models for use in endometriosis research. Acta obstetricia et gynecologica Scandinavica, 96, 644-658 (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).

Research Interests

Endometriosis illustration
Figure 1: The endometrial lining is refluxed through the fallopian tubes into the peritoneal cavity during a phenomenon known as ‘retrograde menstruation’. In 10% of women this material attaches to the lining of the peritoneum to form lesions that characterise the disorder endometriosis. Histological analysis of endometriosis lesions reveals glandular and stromal ‘hallmarks’ similar to the eutopic endometrium. Image provided by Gemma Rundell.

Endometriosis is a chronic oestrogen-dependent inflammatory disease that affects 6-10% of women of reproductive age. It is associated with debilitating pelvic pain, painful periods, and pain during sexual intercourse. It has a significant impact on health-related quality of life and has been estimated to cost the UK £11.7 billion per year. Current treatment strategies for endometriosis are restricted to surgical excision of the lesions or suppression of ovarian function to mimic a premature menopause. In up to 75% of cases, symptoms recur after surgery, and long-term ovarian suppression is often ineffective, suppresses fertility and has unwelcome side effects. There is an unmet clinical need for new treatments for endometriosis.

Endometriosis is the growth of the lining of the uterus (endometrium) on areas outside the uterus, typically the lining of the pelvic cavity (peritoneum). The pain associated with endometriosis is believed to be a result of the growth of new small diameter nerve fibres into the ectopic tissue (endometriosis lesions). We hypothesise that macrophages play a critical role in promoting nerve fibre growth into lesions and activating these nerve fibres thus contributing to endometriosis-associated pain.

The main aims of the research group are:

  1. To characterise the origin and activation state of macrophages present within endometriosis lesions
  2. To determine how macrophages promote nerve growth into lesions and to understand how macrophages activate nerve fibres and contribute to endometriosis-associated pain
  3. To determine how macrophages contribute to central sensitisation and hyperalgesia in endometriosis
  4. To identify new therapeutic targets for endometriosis-associated pain

We hope to shed new light on disease processes that cause endometriosis-associated pain and to contribute to the development of new therapies that may help improve the quality of life for millions of women that suffer from this chronic condition.

Grants

  • MRC Project Grant, ‘Identifying disease promoting macrophages and tissue-identity in endometriosis’, E Greaves (PI), Stephen Jenkins, Andrew Horne, Philippa Saunders,£692,262  (Nov 2018- Dec 2021)

  • Endometriosis Foundation of America,  'A single cell discovery project to compare mouse models of endometriosis and shed light on different theories for the etiology of endometriosis’, E Greaves (PI), $25,000 (2018-2019)

  • Royal Society International Exchanges Cost Share (Taiwan), ‘Using ribosome biogenesis as a therapeutic target for treating endometriosis and the associated complications’, E Greaves (PI), Jim Jinn-Chyuan Sheu, £12,000 (2018-2020)

  • Rosetree’s Trust Research Grant, ‘Macrophage-derived insulin-like growth factor-1: (IGF-1): a key mediator of endometriosis-associated pain? E Greaves (PI), £40,000 (2018-2020)

  • Edinburgh Cellular Genomics Consortium pump-priming competition for single cell transcriptomics, £15,000 (2017 - 2018)
  • Wellbeing of Women Project Grant, ‘Novel repurposing of anticancer drugs to treat endometriosis'. AW Horne (PI), PTK Saunders, P Fowler, C Becker, D Hapangama, K Zondervan, S Sundar, MC Jones, E Greaves, £198,864 (2016 - 2018 )
  • MRC MICA, ‘CB2 agonists as a novel treatment for women with endometriosisassociated pain’. PTK Saunders (PI), AW Horne, E Greaves, £302,097 (2016 - 2018)
  • European Commission Marie Skłodowska-Curie Actions, Research and Innovation Staff Exchange (RISE) Call: H2020-MSCA-RISE-2015  ‘MOMENDO’ (January 2016-December 2020) Co-I with colleagues from Edinburgh, Germany, Sweden, Argentina and Chile
  • The Carnegie Trust Research Incentives Grant ‘Defining the neurogenic signature of the endometriosis-associated macrophage’   £7217 (January 2016-December 2016)
  • MRC Career Development Award ‘Neuroinflammation in endometriosis; macrophages behaving badly? £1,164,455 (January 2015-December 2019)
  • Royal Society International Exchange Scheme £3000 (January-March 2015)
  • Society for Endocrinology Practical Skills Grant £2000 (January-March 2015)

Visit the Society for Endocrinology website

  • Society for Endocrinology Early Career Grant £9360 (2013-2014)
  • Moray Endowment Fund £2000 (2013)
  • MRC Centenary Fund £10800 (2013)

Lab members

  • Dr Ashley Dorning, Postdoc
  • Chloe Hogg, PhD student

Collaborators

  • Professor Philippa Saunders (Centre for Inflammation Research)
  • Professor Andrew Horne (Centre for Reproductive Health)
  • Dr Brett McKinnon (Bern, Switzerland)
  • Professor Sue Fleetwood-Walker (Centre for Integrative Physiology)
  • Dr Louise Hull (University of Adelaide)
  • Professor Sarah Robertson (University of Adelaide)
  • Dr Sylvia Mechsner (Charité, Berlin)

Industry Funding

  • Ferring Pharmaceutics – collaboration