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Research Paper|Volume 11, Issue 9|pp 2653—2669

Prostate enlargement and altered urinary function are part of the aging process

Teresa T. Liu1,2, Samuel Thomas3, Dalton T. Mclean1,4, Alejandro Roldan-Alzate2,5,6, Diego Hernando6,7, Emily A. Ricke1, William A. Ricke1,8
  • 1Department of Urology, University of Wisconsin – Madison, Madison, WI 53705, USA
  • 2K12 Kure, University of Wisconsin – Madison, Madison, WI 53706, USA
  • 3Molecular and Environmental Toxicology, University of Wisconsin – Madison, Madison, WI 53706, USA
  • 4Cancer Biology, University of Wisconsin – Madison, Madison, WI 53706, USA
  • 5Department of Mechanical Engineering, University of Wisconsin – Madison, Madison, WI 53706, USA
  • 6Department of Radiology, University of Wisconsin – Madison, Madison, WI 53705, USA
  • 7Department of Medical Physics, University of Wisconsin – Madison, Madison, WI 53705, USA
  • 8George M. O’Brien Center of Research Excellence, University of Wisconsin – Madison, Madison, WI 53705, USA
Received: March 8, 2019Accepted: April 24, 2019Published: May 13, 2019
https://doi.org/10.18632/aging.101938

Copyright: Liu et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Prostate disease incidence, both benign and malignant, directly correlates with age. Men under 40 years of age are rarely diagnosed with benign or malignant prostate disease, while 90% of men over the age of 80 have histological evidence of benign disease (benign prostatic hyperplasia; BPH). Although rodent models have been invaluable in the study of disease progression and treatment efficacy, the effect of age is often not considered. In examining aged (24-month-old) mice, we observed changes within the lower urinary tract that is typically associated with lower urinary tract dysfunction (LUTD) similar to models of BPH. In this study, we identify LUTD using functional testing as well as various imaging technologies. We also characterize the histological differences within the lower urinary tract between young (2-month-old) and aged mice including proliferation, stromal remodeling, and collagen deposition. Additionally, we examined serum steroid hormone levels, as steroid changes drive LUTD in mice and are known to change with age. We conclude that, with age, changes in prostate function, consistent with LUTD, are a consequence. Therapeutic targeting of endocrine and prostatic factors including smooth muscle function, prostate growth and fibrosis are likely to reestablish normal urinary function.