Endometrial Gap Junction Expression - Early Indicators of Endometriosis and Integral to Invasiveness

Chun-Wei Chen, Jeffery Chavez, Li‐Ling Lin, Chiou‐Miin Wang, Ya‐Ting Hsu, Matthew J. Hart, Jianhua Ruan, Laurel Gillette, Richard O. Burney, Robert S. Schenken, Randal D. Robinson, Maria Gaczyńska, Paweł A. Osmulski, Nameer B. Kirma, Bruce J. Nicholson
In: bioRxiv · 2021 · doi:10.1101/2021.01.25.428135 · W3122826490
preprint OA: green CC0 ⤵ 1 in-corpus citation
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Endometrial single-cell profiling revealed altered connexin and gap junction expression, inducing mesothelial barrier breakdown and enabling peritoneal invasion in endometriosis patients.

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Abstract

Abstract Endometriosis is an invasive disease, and a leading cause of pain, infertility and disability among women, with an incidence 10 fold that of cancer. A more complete understanding of disease pathogenesis is essential for the development of non-surgical diagnostic assays and non-hormonal therapeutics. Avoidance of immune clearance and implantation of endometrial tissue on peritoneal surfaces are features of endometriosis lesion formation that overlap with cancer metastasis. Connexins, and the gap junctions they form, have been implicated in cancer progression, and may be associated endometriosis pathophysiology. Single cell transcriptomic profiling of endometrial epithelial and stromal cells from women with endometriosis reveals a striking and progressive shift in expression of connexins and related regulatory and junctional genes. We demonstrate that gap junction coupling between endometrial cells and the peritoneal mesothelium is dramatically induced, specifically in endometriosis patients, and is required for invasion by inducing breakdown of the mesothelial barrier function.

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endometriosisinfertility

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