# Osteopontin: A Novel Mediator of prostatic inflammation and fibrosis

> **NIH NIH K01** · EASTERN VIRGINIA MEDICAL SCHOOL · 2022 · $72,040

## Abstract

PROJECT SUMMARY/ABSTRACT
 The overarching goal of my proposal is to acquire technical and professional skills to become an
independent investigator at a leading academic institution and develop a research program deciphering the
molecular mechanism of inflammation induced prostatic tissue remodeling and fibrosis. This will be pursued
through a scientific project that will determine whether osteopontin, a pro-fibrotic secreted phosphoprotein,
stimulates prostatic inflammation, fibrosis, and lower urinary tract dysfunction.
 My training is focused on four key areas: 1) functional testing of mouse urinary function, 2) developing
biomedical engineering technologies to study prostatic fibrosis in vitro, 3) testing and further developing animal
models to study inflammation-induced prostatic fibrosis and its consequences on urinary function and, 4)
gaining essential training in immune-regulated tissue remodeling. UW-Madison and the UW O`Brien Center for
Benign Urology Research presents a unique environment for the proposed research and career development
activities. This includes seminars presented by local and national leaders of the field, career development
activities of several institutes across campus, clinical training of the Department of Urology, and specific
training in immunopathology and tissue engineering.
 Lower urinary tract symptoms (LUTS) secondary to benign prostatic diseases deteriorate the quality of
life as men age. The treatment of male LUTS costs $4 billion annually and presents an economic burden on
our healthcare system. It has been recently identified that prostatic inflammation and fibrosis are associated
with LUTS, but the exact contribution of these mechanism to urinary dysfunction is unknown. Medical therapies
targeting inflammation and fibrosis could enhance drug development and provide novel molecular targets for
LUTS. Based on my preliminary studies, I hypothesize that inflammation-induced osteopontin levels stimulate
prostatic fibrosis and lower urinary tract dysfunction (LUTD). The hypothesis will be tested by the following
aims:
 1) Test the hypothesis that OPN is required for inflammation-induced prostatic collagen accumulation
 and LUTD,
 2) Test the hypothesis that OPN induces prostatic fibrosis.
 The proposal will provide novel detection of collagen deposition, 3D in vitro and in vivo models of
prostatic fibrosis. It will also decipher the specific role of inflammation-induced prostatic fibrosis in lower urinary
tract dysfunction. This will be achieved by capitalizing on recently established prostatic inflammation models
and state-of-the-art urinary physiological tests uniquely available at the UW-Madison.

## Key facts

- **NIH application ID:** 10694242
- **Project number:** 7K01DK127150-03
- **Recipient organization:** EASTERN VIRGINIA MEDICAL SCHOOL
- **Principal Investigator:** PETRA POPOVICS
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $72,040
- **Award type:** 7
- **Project period:** 2021-01-15 → 2025-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10694242

## Citation

> US National Institutes of Health, RePORTER application 10694242, Osteopontin: A Novel Mediator of prostatic inflammation and fibrosis (7K01DK127150-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10694242. Licensed CC0.

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