Prostate fibrosis contributes to lower urinary tract dysfunction (LUTD). To develop targeted treatments for prostate fibrosis, it is necessary to identify the cell types and molecular pathways required for collagen production. We used a genetic approach to label and track potential collagen-producing cell lineages in mouse prostate through a round of Escherichia coli UTI89-mediated prostate inflammation. E. coli increased collagen density and production in Gli1+, S100a4+, Lyz2+ and Cd2+ cell lineages, but not in Myh11+ or Srd5a2+ cell lineages, in the mouse prostate. Molecular phenotyping revealed GLI1+LYZ+S100A4+ cells (fibrocytes) in histologically inflamed human prostate. These fibrocytes colocalized with regions of increased collagen in men with LUTD. Fibrocyte recruitment and collagen synthesis was impaired in Ccr2 null mice but restored by allotransplantation of Rosa-GFP donor bone marrow-derived cells. These results suggest that bone marrow-derived fibrocytes are a mediator of prostatic collagen accumulation.
Keywords: CCR2; Fibrocyte; Fibrosis; LUTD; Myofibroblast; Prostate.
© 2025. Published by The Company of Biologists.