# Prostate inflammation increases collagen and voiding dysfunction

> **NIH NIH F30** · UNIVERSITY OF WISCONSIN-MADISON · 2022 · $39,129

## Abstract

Project Summary/Abstract
Few veterinary clinicians pursue a career in urologic research despite working with patients that develop
spontaneous voiding dysfunction. The applicant is a uniquely qualified candidate, having a veterinarian’s
understanding of animal models, access to patients prone to spontaneous urinary dysfunction, and the basic
urologic research training few veterinarians receive.
The goal of this fellowship is to provide the applicant with training for a successful career as a veterinary
pathologist and translational researcher. The training plan accomplishes this goal by building research study
design skills, a strong background in the primary literature, proficiency in basic histopathology, and foundational
veterinary knowledge and clinical skills. In addition, the training plan fosters key professional development
opportunities by building proficiency in laboratory business skills, mentorship, collaboration, communication,
and grantsmanship. The plan includes specific activities for each segment of the applicant’s training and progress
will be evaluated by the applicant’s sponsor and thesis committee.
The proposed research focuses on prostatic collagen accumulation, which is linked to bothersome lower urinary
tract symptoms (LUTS) in aging men. Men with LUTS often have increased frequency and urgency to urinate,
difficulty initiating urination, incomplete bladder emptying, decreased urine stream force, and interruption of
stream, symptoms that decrease quality of life and for which health care is costly. Mechanisms for prostatic
collagen accumulation in humans and canines remain unknown but inflammation has been linked to collagen
accumulation. In particular, prostatic interleukin-1-beta (IL-1β) abundance has been correlated with LUTS in
men. IL-1β is a mediator of inflammatory responses, and prostatic expression of IL-1β can be manipulated in
genetically engineered mice. This training plan will use these genetically engineered mice to test the overarching
hypothesis that prostatic IL-1β drives inflammation, fibrosis and voiding dysfunction.
The University of Wisconsin-Madison is the ideal environment to conduct these studies because it is the home
of an NIH-designated O’Brien Center for Excellence in Benign Urologic Research, one of only three focused on
prostate-related disease. The UW-Madison O’Brien Center provides an unparalleled rodent urinary function
testing core facility, bimonthly speakers, and numerous opportunities for collaboration. The sponsor of this
work, Dr. Vezina, is also a longstanding contributor to the NIDDK-sponsored Genitourinary Development
Molecular Anatomy Project (GUDMAP), bringing expertise on detailed molecular mapping, training that will be
needed to complete the research aims and throughout the applicant’s career. UW-Madison also has a Veterinary,
Pharmacy, and School of Medicine on the same campus, providing access to clinically relevant species, unique
resources and further collaborations.

## Key facts

- **NIH application ID:** 10476322
- **Project number:** 5F30DK122686-04
- **Recipient organization:** UNIVERSITY OF WISCONSIN-MADISON
- **Principal Investigator:** Hannah Margaret Ruetten
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $39,129
- **Award type:** 5
- **Project period:** 2019-09-15 → 2023-06-14

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10476322

## Citation

> US National Institutes of Health, RePORTER application 10476322, Prostate inflammation increases collagen and voiding dysfunction (5F30DK122686-04). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10476322. Licensed CC0.

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