Abstract
Aging is associated with loss of tissue mass and a decline in adult stem cell function in many tissues. In contrast, aging in the prostate is associated with growth-related diseases including benign prostatic hyperplasia (BPH). Surprisingly, the effects of aging on prostate epithelial cells have not been established. Here we find that organoid-forming progenitor activity of mouse prostate basal and luminal cells is maintained with age. This is caused by an age-related expansion of progenitor-like luminal cells that share features with human prostate luminal progenitor cells. The increase in luminal progenitor cells may contribute to greater risk for growth-related disease in the aging prostate. Importantly, we demonstrate expansion of human luminal progenitor cells in BPH. In summary, we define a Trop2+ luminal progenitor subset and identify an age-related shift in the luminal compartment of the mouse and human prostate epithelium. Aging is a significant risk factor for BPH and prostate cancer, but how aging increases disease risk in the prostate remains poorly defined. Crowell et al. show that progenitor-enriched luminal cells are expanded with aging in the mouse and human prostate, and may contribute to BPH.
Original language | English (US) |
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Pages (from-to) | 1499-1510.e6 |
Journal | Cell Reports |
Volume | 28 |
Issue number | 6 |
DOIs | |
State | Published - Aug 6 2019 |
Externally published | Yes |
Keywords
- aging
- basal
- epithelium
- luminal
- organoid
- progenitor
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology