Journal
SCIENTIFIC REPORTS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep44169
Keywords
-
Categories
Funding
- MRC Programme Grant [G1100356/1]
- MRC Career Development Award [MRC MR/M009238/1]
- BBSRC [BB/G002738/1] Funding Source: UKRI
- MRC [MR/M009238/1, G0901697, MR/P00265X/1, MR/N024524/1, G1100356] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/G002738/1] Funding Source: researchfish
- Medical Research Council [G1100356, MR/P00265X/1, MR/N024524/1, MR/M009238/1, G0901697] Funding Source: researchfish
- Wellbeing of Women [RG1436, RG1956] Funding Source: researchfish
Ask authors/readers for more resources
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 PGE(2)-signaling pathway (including COX-2, EP2, EP4) in endometriosis lesions, dorsal root ganglia (DRG), spinal cord, thalamus and forebrain. TRPV1, a PGE(2)-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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available