Pain is a common endometriosis symptom, but it is still unclear what causes it.
Chinese researchers discovered that a protein on the surface of endometrium cells may help promote endometriosis-associated pain.
The team discussed its findings about the P2X3 protein in a study titled “P2X3 receptor involvement in endometriosis pain via ERK signaling pathway.” The article was published in the journal PLoS ONE.
Scientists say an increase in the number of nerve fibers in the endometrium — the layer that lines the inside of the uterus — and endometriotic lesions contribute to the pain the disease generates. They also link the pain to another hallmark of the condition: inflammed nerve fibers.
In addition, researchers know that inflammation-promoting signals can activate cell surface proteins in ways that trigger pain. These proteins include TRPV1 channels and P2X3 receptors.
Previous studies have demonstrated that TRPV1 levels are increased in endometriosis lesions and that these levels correlate with pain. Scientists did not know until the Chinese study if the P2X3 receptor was connected with endometriosis pain, however.
Researchers at the Zhejiang University School of Medicine’s Women Hospital analyzed tissue samples from women who had laparoscopic surgery for endometriosis, infertility or tubal ligation to see if P2X3 played a role in endometriosis pain. Tubal ligation is commonly referred to as having your tubes tied.
The study, conducted between June 2013 and July 2014, covered 65 women, 48 with endometriosis and 17 without it. Twenty-seven, or 56 percent, of the women with endometriosis complained of pain, while none of those without it were experiencing pain. Researchers used patients’ answers on a questionnaire to assign pain scores to them.
The team found significantly higher levels of P2X3 in the endometrium and lesions of endometriosis patients than in the endometrium tissue of the control group. When they correlated the protein’s levels with pain, they found a connection between increased levels of P2X3 in the endometrium and endometriotic lesions and the severity of pain that patients reported.
These results showed that “P2X3 in endometriotic lesions and endometriosis endometrium imply an important role in the mechanisms of endometriosis-associated pain triggering,” they wrote.
The team confirmed in laboratory experiments that activating P2X3 receptors could trigger cascades of pain-related signaling.
“In summary, our preliminary results showed that increased P2X3 expression in endometriotic lesions is correlated with endometriosis pain, and P2X3 might be involved in endometriosis pain signal” transmission, they wrote. Additional studies are needed to confirm the findings, they added.