Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia

Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia

Clinical and experimental evidence has linked Benign Prostatic Hyperplasia (BPH) with dyslipidemic and hypercholesterolemic conditions, though the underlying cellular mechanisms remain unclear. This study investigates the impact of dyslipidemia, specifically oxidized LDL (OxLDL), on prostatic stroma...

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Bibliographic Details
Published in:Biology (Basel, Switzerland) Vol. 13; no. 10; p. 827
Main Authors: Roldán Gallardo, Franco F, Martínez Piñerez, Daniel E, Reinarz Torrado, Kevin F, Berg, Gabriela A, Herzfeld, Jael D, Da Ros, Vanina G, López Seoane, Manuel, Maldonado, Cristina A, Quintar, Amado A
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 16-10-2024
MDPI
Subjects:
Atherosclerosis
Carbohydrates
Cell cycle
Cell growth
Cell interactions
Cell proliferation
Cholesterol
Diabetes mellitus
Diet
Dyslipidemia
Ethylenediaminetetraacetic acid
Extracellular vesicles
High fat diet
Hypercholesterolemia
Hyperplasia
Hypertrophy
Inflammation
Laboratory animals
Low density lipoprotein
Low density lipoproteins
Metabolic disorders
Metformin
Microscopy
Oxidation
Oxidative stress
Prostate
prostate hyperplasia
Stromal cells
Argentina
St Louis Missouri
United States > US
metformin
extracellular vesicles
dyslipidemia
prostate hyperplasia
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Summary:Clinical and experimental evidence has linked Benign Prostatic Hyperplasia (BPH) with dyslipidemic and hypercholesterolemic conditions, though the underlying cellular mechanisms remain unclear. This study investigates the impact of dyslipidemia, specifically oxidized LDL (OxLDL), on prostatic stromal cell proliferation and the release of extracellular vesicles (EVs). Mice were fed a high-fat diet, and human prostatic stromal cells (HPSCs) were treated with OxLDL. Proliferation assays and EV characterization were performed to assess the role of EVs in BPH progression. Pro-atherogenic conditions significantly increased cell proliferation in both murine prostatic cells and HPSCs. Treatment with metformin effectively inhibited OxLDL-induced proliferation. Additionally, OxLDL stimulated the production and release of pro-proliferative EVs by HPSCs, which further promoted cellular proliferation. The findings suggest that dyslipidemia drives prostatic stromal cell proliferation and EV secretion, contributing to BPH progression. Metformin demonstrates potential as a therapeutic agent to mitigate these effects, offering insight into novel strategies for BPH management. This study highlights the complex interaction between dyslipidemia, cell proliferation, and extracellular communication in the context of BPH pathogenesis.
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ISSN:2079-7737
2079-7737
DOI:10.3390/biology13100827