Increased α2-6 sialylation of endometrial cells contributes to the development of endometriosis

Abstract

Endometriosis: a sweet and sticky mechanism uncovered A growth factor involved in cell differentiation and proliferation contributes to the development of endometriosis by stimulating a protein modification mechanism that increases the adhesiveness of cells lining the uterus. Endometriosis results when these cells, known as endometrial cells, start growing outside the uterus causing pelvic pain, heavy periods and, in some cases, infertility. Ki-Tae Ha at Pusan National University, Yangsan, South Korea, and colleagues found that transforming growth factor-β1 signaling promoted the addition of sialic acid sugar units onto endometrial cell surface proteins. This modification enhanced the adhesion of endometrial cells to mesothelial cells, which line other internal organs, and the formation of endometriosis lesions in mice. Preventing sialic acid binding to its mesothelial cell receptor reduced lesion formation. The findings reveal a new molecular mechanism underlying endometriosis and a potential treatment strategy.