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The role of estrogen receptor alpha in prostatic fibrosis contributing to benign prostatic hyperplasia

Award Number: F31DK135376
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

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The role of estrogen receptor alpha in prostatic fibrosis contributing to benign prostatic hyperplasia - Project Abstract Benign prostatic hyperplasia (BPH) is a disease impacting much of the aging male population, affecting 50% of men 50 and older, and increasing to 90% of men 80 and older. The etiology of BPH is complex and multifactorial, though proliferation, smooth muscle dysfunction and fibrosis within the prostate are often considered the largest contributing factors, in addition to age. Estrogen signaling via receptors (ERs) within the prostate have been shown to play conflicting roles, with ERα associated with increased proliferation while ERβ with apoptotic processes. Current BPH therapeutic strategies target androgen biosynthesis without considering that androgens are regularly converted to estrogenic ligands in the steroid hormone signaling pathway. I hypothesize that estrogen signaling within the prostate, specifically ERα activity, induces prostatic fibrosis and thus contributes to the development of lower urinary tract dysfunction (LUTD) and BPH. I aim to evaluate this hypothesis through the use of mass spectrometry (MS)-based proteomics analyses. With the development of high resolution and accurate mass instrumentation, MS has become the preferred technique for deep, targeted and global proteomic profiling investigations. In addition, the development of mass spectrometry imaging (MSI) allows for high throughput analysis of protein and peptide species in a biological tissue with no prior knowledge, thus obtaining critical spatial information of hundreds of analytes in a single imaging run. I plan to utilize the high sensitivity and selectivity of both MSI and traditional chromatography-based LC-MS/MS experiments to reach the following goals: 1) to determine if ERα agonism in mice promotes prostatic fibrosis and LUTD and 2) to uncover if loss of ERα function decreases prostatic fibrosis in vivo. Collectively, these aims will both facilitate the use of MS-based strategies in urologic research and yield novel insights into the complex roles that estrogen receptor alpha plays within the prostate.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2024 ( Subtotal = $37,627 )
2024	2024	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	2	5/10/2024	NON-COMPETING CONTINUATION	$1,280
2024	2024	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	2	3/20/2024	NON-COMPETING CONTINUATION	$36,347
														Subtotal = $37,627

Issue Date FY: 2023 ( Subtotal = $36,347 )
2023	2023	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	1	3/13/2023	NEW	$36,347
2023	2023	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	1	3/13/2023	NEW	$0
														Subtotal = $36,347

Grand Total All Awards = $73,974

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The role of estrogen receptor alpha in prostatic fibrosis contributing to benign prostatic hyperplasia

Award Number: F31DK135376

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

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