Profiles

Courses Taught

• Molecules to Cells

Graduate Education

• MS in Biological Sciences, University of Pecs, Hungary
• PhD, University of St. Andrews, UK

Postdoctoral Education

• University of Miami/Miami VA Medical Center
• Case Western Reserve University
• K12/K01 Scholar, University of Wisconsin-Madison

Lab Location

Lester Hall, Room 445

Research Interests

Our mission is to improve the medical treatment of Lower Urinary Tract Symptoms (LUTS) in aging men that are linked to benign prostate disease. LUTS represent a cluster of urinary problems that affects the aging male population worldwide significantly deteriorating their quality of life. Our limited knowledge on the disease pathology prevents us from developing more efficacious therapies. Our goal is to identify the molecular mechanism of inflammation-induced pathological changes in the prostate through translational research and the development of animal and cellular models.

Foam cells in prostate pathology

We recently discovered that macrophages migrate to the prostate lumen and differentiate into foam cells via lipid droplet accumulation in a mouse model of lower urinary tract dysfunction (LUTD). Our research aims to understand the molecular mechanism of this process as well as its effects on disease progression. (more information: https://pathsocjournals.onlinelibrary.wiley.com/doi/abs/10.1002/path.6074)

Pro-inflammatory signals in prostate disease

Expressional analysis of prostates from mice with steroid hormone-induced LUTD identified serum amyloid A (SAA1/2) and osteopontin as key upregulated pro-inflammatory genes. Our studies suggest that osteopontin is important for macrophage infiltration, epithelial proliferation and fibrosis. Future studies will further examine the role of osteopontin via testing an antagonistic therapy as well as its overexpression in prostate regeneration experiments.

In contrast, there is much less known about the role of SAAs. Our current studies aim to decipher whether there is an increased SAA level in LUTS/BPH prostates as well as determine its downstream signaling and physiological role in the prostate.

Keywords: prostate, inflammation, fibrosis, macrophage differentiation

Relevant Publications

• Popovics P, Awadallah WN, Kohrt S, Case TC, Miller NL, Ricke E, Huang W, Ramirez-Solano M, Liu Q, Vezina CM, Matusik RJ, Ricke WA, Grabowska MM. Prostatic osteopontin expression is associated with symptomatic benign prostatic hyperplasia. The Prostate. 2020; 80:731-741.
• Popovics P, Skalitzky KO, Schroeder E, Jain A, Silver SV, Van Fritz F, Uchtmann KS, Vezina CM, Ricke WA. Steroid hormone imbalance drives macrophage infiltration and Spp1/osteopontin+ foam cell differentiation in the prostate. J Pathol. 2023;260:177-189.
• Popovics P, Jain A, Skalitzky KO, Schroeder E, Ruetten HM, Cadena M, Uchtmann KS, Vezina CM, Ricke WA. Osteopontin deficiency leads to the resolution of prostatic fibrosis and inflammation. Int J Mol Sci. 2021; 18:22:12461.
• Popovics P, Cai R, Sha W, Rick FG and Schally AV. Growth hormone-releasing hormone antagonists reduce prostatic enlargement and inflammation in carrageenan-induced chronic prostatitis. The Prostate. 2018; 78: 970-980.
• Popovics P, Schally AV, Salgueiro L, Kovacs K and Rick FG. Antagonists of growth hormone-releasing hormone (GHRH) inhibit proliferation induced by inflammation in prostatic epithelial cells. Proceedings of the National Academy of Sciences of the United States of America. 2017; 114(6):1359-1364.

Publication list

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