A protein called CXCR7 was identified as a potential nonhormonal therapeutic target for endometriosis after researchers discovered that it is overproduced in patients with the disease, when then leads to more inflammation.
Findings were published in the study, “G-Protein-Coupled Receptor CXCR7 Is Overexpressed in Human and Murine Endometriosis,” which appeared in the journal Reproductive Sciences.
Endometriosis is caused by the movement of endometrial tissue from a woman’s uterus into an external area such as the peritoneal cavity or the abdomen, resulting in inflammation and pain.
Chemokines are small proteins secreted by different cell types that bind to specific chemokine receptors present on cells. Upon binding, they are able to carry out their functions, many of which are related to immunity and inflammation.
One particular chemokine — CXCL12 — binds to a receptor called CXCR4. CXCL12- CXCR4 signaling is increased in women with endometriosis. A recent study also identified another receptor — CXCR7 — as a second receptor for CXCL12.
CXCR7 expression is increased in pathological inflammation and tumor development and, therefore, may play a part in inflammation associated with endometriosis. Researchers in this study focused on clarifying CXCR7’s role in human endometriosis and in a mouse model of endometriosis.
First, they investigated the expression and location of CXCR7 in human endometriosis. Results showed that the normal endometrium has very low expression of CXCR7, with no changes across the different phases of the menstrual cycle. However, CXCR7 was found to be significantly increased in endometriosis, with high levels specifically in the glands and associated blood vessels.
Next, researchers induced endometriosis in mice and found that CXCL12 levels increased gradually from the day of endometriosis induction, with a peak on the 15th day, and then lowered after 30 days. And again, levels of CXCR7 were much higher in the uteri of mice with endometriosis than in normal mice.
“We found out an overexpression of this G-protein-coupled receptor CXCR7 in endometriosis patients,” corresponding author Ramanaiah Mamillapalli, PhD, a research scientist at the Yale School of Medicine, said in a Yale News story. “Then we looked at what its function in mice is, and we found that it enhanced the proliferation of cells that cause cell division. It also affects apoptosis or cell death. So it will inhibit the cell death. And then we are communicating one more manuscript in which we inhibited this molecule, and there, you can see the lesion size reduced very much.”
The authors of the study conclude: “Specific upregulation of CXCR7 in different cellular populations of endometriosis microenvironment may represent a novel target for new nonhormonal treatments of this chronic inflammatory disease.”
Finding possible alternative therapies for treating endometriosis is important because hormonal treatments can be overpowering and lead to significant side effects.
The research team also is now developing diagnostic tools to detect endometriosis through the use of small molecules called microRNAs. Right now, it can take a long time for women to be diagnosed because there is no diagnostic tool to detect the disease besides surgery.
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