Study Sheds Light on the Molecular Mechanism of Endometriosis Lesion Formation

Researchers found that a protein called NOD1 is overproduced by ectopic cells.

Key Points

Highlights: 

• Researchers identified a new protein that may be involved in the progression of endometriotic lesions.

Importance:

• This finding may open up new avenues for developing novel therapies to treat the disease in the future.

What’s done here:

• The team analyzed the expression of the protein called NOD1 in tissues and mesenchymal stem cells obtained from eutopic endometrium and endometriosis.

Key results:

• NOD1 expression was higher in ectopic mesenchymal stem cells from endometriosis compared to the normal endometrium.
• The expression of interleukin-8 was higher in the ectopic mesenchymal stem cells compared to eutopic mesenchymal stem cells. 
• Treatment with a NOD1 agonist led to an increase in the proliferation, invasion, and migration of the eutopic mesenchymal stem cells.
• NOD1 inhibition led to a significant reduction in the proliferation, clone formation, invasion, and migration of ectopic mesenchymal stem cells.

Limitations:

• These are early findings and more research is needed to shed light on the mechanism of action of NOD1 expression.

Lay Summary

The production of a protein called Nucleotide-binding Oligomerization Domain 1 (NOD1) in ectopic mesenchymal stem cells may be associated with the formation of ectopic endometrial lesions, according to a new study published in the International Journal of Stem Cells.

This finding sheds light on the potential mechanism of endometriosis formation and progression and may help researchers develop new treatments against the disease in the future.

To study the potential role of NOD1 in ectopic endometrial lesions, a team of researchers from China led by Dr. Yuanyuan Zhang of the Department of Gynecologic Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital at the Chinese Academy of Medical Sciences & Peking Union Medical College in Beijing obtained tissues and mesenchymal stem cells from eutopic endometrium and endometriosis.

They then assessed the expression of NOD1 and measured the quantity of different cell signaling molecules involved in immunity.  They found that the levels of NOD1 protein were higher in ectopic mesenchymal stem cells from endometriosis compared to the lining of the uterus. Moreover, the expression of the cell signaling molecule interleukin-8 was also higher in the ectopic mesenchymal stem cells compared to eutopic mesenchymal stem cells. 

When they treated the cells with a NOD1 agonist, the proliferation, invasion, and migration of the eutopic mesenchymal stem cells was significantly increased.  On the contrary, inhibiting NOD1 led to a significant reduction in the proliferation, clone formation, invasion, and migration abilities of the ectopic mesenchymal stem cells. However, it does not affect their capacity for programmed cell death.

The researchers concluded that NOD1 may play a role in the progression of endometriosis.

NOD1 is a cytosolic pattern recognition receptor, which plays a key role in the innate immune response.

Research Source: https://pubmed.ncbi.nlm.nih.gov/38531608/