Cellular heterogeneity of human fallopian tubes in normal and hydrosalpinx disease states identified by scRNA-seq

• Published in: Developmental cell Vol. 57; no. 7; pp. 914 - 929.e7
• Main Authors: Ulrich, Nicole D, Shen, Yu-chi, Ma, Qianyi, Yang, Kun, Hannum, D. Ford, Jones, Andrea, Machlin, Jordan, Randolph, John F., Smith, Yolanda R., Schon, Samantha B., Shikanov, Ariella, Marsh, Erica E., Lieberman, Richard, Gurczynski, Stephen J., Moore, Bethany B., Li, Jun Z., Hammoud, Sue
• Format: Journal Article
• Language: English
• Published: 22-03-2022
• ISSN: 1534-5807; 1878-1551
• DOI: 10.1016/j.devcel.2022.02.017

Fallopian tube (FT) homeostasis requires dynamic regulation of heterogeneous cell populations and is disrupted in infertility and ovarian cancer. Here we applied single-cell RNA-seq to profile 59,738 FT cells from 4 healthy pre-menopausal subjects. The resulting cell atlas contains 12 major cell types representing epithelial, stromal and immune compartments. Re-clustering of epithelial cells identified 4 ciliated and 6 non-ciliated secretory epithelial subtypes, two of which represent potential progenitor pools: one leading to mature secretory cells, while the other contributing to either ciliated cells or one of the stromal cell types. To understand how FT cell numbers and states change in a disease state, we analyzed 17,798 cells from two hydrosalpinx samples and observed shifts in epithelial and stromal populations, and cell type-specific changes in extracellular matrix and TGF-β signaling, underscoring fibrosis pathophysiology. This resource is expected to facilitate future studies to understand fallopian tube homeostasis in normal development and disease.
Fallopian tube homeostasis requires dynamic regulation of heterogeneous cell populations, which are disrupted in disease. Ulrich et. al apply single-cell RNA sequencing to untangle cellular heterogeneity within healthy and disease samples, identifying major cell types, epithelial subtypes, cell population shifts, and cell type-specific transcriptomic changes in disease states.