Decoding the endometrial niche of Asherman’s Syndrome at single-cell resolution

Xavier Santamaria (), Beatriz Roson, Raul Perez-Moraga, Nandakumar Venkatesan, Maria Pardo-Figuerez, Javier Gonzalez-Fernandez, Jaime Llera-Oyola, Estefania Fernández, Inmaculada Moreno, Andres Salumets, Hugo Vankelecom, Felipe Vilella and Carlos Simon ()
Additional contact information
Xavier Santamaria: Carlos Simon Foundation, INCLIVA Health Research Institute
Beatriz Roson: Carlos Simon Foundation, INCLIVA Health Research Institute
Raul Perez-Moraga: Carlos Simon Foundation, INCLIVA Health Research Institute
Nandakumar Venkatesan: University of Valencia
Maria Pardo-Figuerez: Carlos Simon Foundation, INCLIVA Health Research Institute
Javier Gonzalez-Fernandez: Carlos Simon Foundation, INCLIVA Health Research Institute
Jaime Llera-Oyola: Carlos Simon Foundation, INCLIVA Health Research Institute
Estefania Fernández: Carlos Simon Foundation, INCLIVA Health Research Institute
Inmaculada Moreno: Carlos Simon Foundation, INCLIVA Health Research Institute
Andres Salumets: University of Tartu
Hugo Vankelecom: University of Leuven (KU Leuven)
Felipe Vilella: Carlos Simon Foundation, INCLIVA Health Research Institute
Carlos Simon: Carlos Simon Foundation, INCLIVA Health Research Institute

Nature Communications, 2023, vol. 14, issue 1, 1-15

Abstract: Abstract Asherman’s Syndrome is characterized by intrauterine adhesions or scarring, which cause infertility, menstrual abnormalities, and recurrent pregnancy loss. The pathophysiology of this syndrome remains unknown, with treatment restricted to recurrent surgical removal of intrauterine scarring, which has limited success. Here, we decode the Asherman’s Syndrome endometrial cell niche by analyzing data from over 200,000 cells with single-cell RNA-sequencing in patients with this condition and through in vitro analyses of Asherman’s Syndrome patient-derived endometrial organoids. Our endometrial atlas highlights the loss of the endometrial epithelium, alterations to epithelial differentiation signaling pathways such as Wnt and Notch, and the appearance of characteristic epithelium expressing secretory leukocyte protease inhibitor during the window of implantation. We describe syndrome-associated alterations in cell-to-cell communication and gene expression profiles that support a dysfunctional pro-fibrotic, pro-inflammatory, and anti-angiogenic environment.

Date: 2023
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DOI: 10.1038/s41467-023-41656-1

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