EP2 receptor antagonism reduces peripheral and central hyperalgesia in a preclinical mouse model of endometriosis

Erin Greaves, Andrew W. Horne, Helen Jerina, Marta Mikolajczak, Lisa Hilferty, Rory Mitchell, Sue M. Fleetwood-Walker, Philippa T. K. Saunders

Research output: Contribution to journalArticlepeer-review

Abstract

Endometriosis is an incurable gynecological disorder characterized by debilitating pain and the establishment of innervated endometriosis lesions outside the uterus. In a preclinical mouse model of endometriosis we demonstrated overexpression of the PGE2-signaling pathway (including COX-2, EP2, EP4) in endometriosis lesions, dorsal root ganglia (DRG), spinal cord, thalamus and forebrain. TRPV1, a PGE2-regulated channel in nociceptive neurons was also increased in the DRG. These findings support the concept that an amplification process occurs along the pain neuroaxis in endometriosis. We then tested TRPV1, EP2, and EP4 receptor antagonists: The EP2 antagonist was the most efficient analgesic, reducing primary hyperalgesia by 80% and secondary hyperalgesia by 40%. In this study we demonstrate reversible peripheral and central hyperalgesia in mice with induced endometriosis.
Original languageEnglish
Article number44169
Number of pages10
JournalScientific Reports
Volume7
DOIs
Publication statusPublished - 10 Mar 2017

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