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

Autores
Roldán Gallardo, Franco Fabián; Martínez Piñerez, Daniel E.; Reinarz Torrado, Kevin F.; Berg, Gabriela Alicia; Herzfeld, Jael Dafne; Da Ros, Vanina Gabriela; López Seoane, Manuel; Maldonado, Cristina A.; Quintar, Amado Alfredo
Año de publicación
2024
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background: 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). Methods: 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. Results: 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. Conclusions: 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.
Fil: Roldán Gallardo, Franco Fabián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Martínez Piñerez, Daniel E.. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Reinarz Torrado, Kevin F.. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Berg, Gabriela Alicia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Herzfeld, Jael Dafne. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Da Ros, Vanina Gabriela. Fundación de Instituto de Biología y Medicina Experimental; Argentina
Fil: López Seoane, Manuel. Sanatorio Allende; Argentina
Fil: Maldonado, Cristina A.. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Quintar, Amado Alfredo. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Materia
VESICULAS EXTRACELULARES
HIPERPLASIA PROSTATICA BENIGNA
METFORMINA
DISLIPIDEMIAS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/265930

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network_name_str CONICET Digital (CONICET)
spelling Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic HyperplasiaRoldán Gallardo, Franco FabiánMartínez Piñerez, Daniel E.Reinarz Torrado, Kevin F.Berg, Gabriela AliciaHerzfeld, Jael DafneDa Ros, Vanina GabrielaLópez Seoane, ManuelMaldonado, Cristina A.Quintar, Amado AlfredoVESICULAS EXTRACELULARESHIPERPLASIA PROSTATICA BENIGNAMETFORMINADISLIPIDEMIAShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Background: 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). Methods: 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. Results: 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. Conclusions: 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.Fil: Roldán Gallardo, Franco Fabián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; ArgentinaFil: Martínez Piñerez, Daniel E.. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; ArgentinaFil: Reinarz Torrado, Kevin F.. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; ArgentinaFil: Berg, Gabriela Alicia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Herzfeld, Jael Dafne. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Da Ros, Vanina Gabriela. Fundación de Instituto de Biología y Medicina Experimental; ArgentinaFil: López Seoane, Manuel. Sanatorio Allende; ArgentinaFil: Maldonado, Cristina A.. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Quintar, Amado Alfredo. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaMDPI2024-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/265930Roldán Gallardo, Franco Fabián; Martínez Piñerez, Daniel E.; Reinarz Torrado, Kevin F.; Berg, Gabriela Alicia; Herzfeld, Jael Dafne; et al.; Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia; MDPI; Biology; 13; 10; 10-2024; 1-152079-7737CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/2079-7737/13/10/827info:eu-repo/semantics/altIdentifier/doi/10.3390/biology13100827info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-17T11:12:53Zoai:ri.conicet.gov.ar:11336/265930instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-17 11:12:53.769CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia
title Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia
spellingShingle Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia
Roldán Gallardo, Franco Fabián
VESICULAS EXTRACELULARES
HIPERPLASIA PROSTATICA BENIGNA
METFORMINA
DISLIPIDEMIAS
title_short Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia
title_full Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia
title_fullStr Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia
title_full_unstemmed Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia
title_sort Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia
dc.creator.none.fl_str_mv Roldán Gallardo, Franco Fabián
Martínez Piñerez, Daniel E.
Reinarz Torrado, Kevin F.
Berg, Gabriela Alicia
Herzfeld, Jael Dafne
Da Ros, Vanina Gabriela
López Seoane, Manuel
Maldonado, Cristina A.
Quintar, Amado Alfredo
author Roldán Gallardo, Franco Fabián
author_facet Roldán Gallardo, Franco Fabián
Martínez Piñerez, Daniel E.
Reinarz Torrado, Kevin F.
Berg, Gabriela Alicia
Herzfeld, Jael Dafne
Da Ros, Vanina Gabriela
López Seoane, Manuel
Maldonado, Cristina A.
Quintar, Amado Alfredo
author_role author
author2 Martínez Piñerez, Daniel E.
Reinarz Torrado, Kevin F.
Berg, Gabriela Alicia
Herzfeld, Jael Dafne
Da Ros, Vanina Gabriela
López Seoane, Manuel
Maldonado, Cristina A.
Quintar, Amado Alfredo
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv VESICULAS EXTRACELULARES
HIPERPLASIA PROSTATICA BENIGNA
METFORMINA
DISLIPIDEMIAS
topic VESICULAS EXTRACELULARES
HIPERPLASIA PROSTATICA BENIGNA
METFORMINA
DISLIPIDEMIAS
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Background: 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). Methods: 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. Results: 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. Conclusions: 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.
Fil: Roldán Gallardo, Franco Fabián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Martínez Piñerez, Daniel E.. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Reinarz Torrado, Kevin F.. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Berg, Gabriela Alicia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Herzfeld, Jael Dafne. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Da Ros, Vanina Gabriela. Fundación de Instituto de Biología y Medicina Experimental; Argentina
Fil: López Seoane, Manuel. Sanatorio Allende; Argentina
Fil: Maldonado, Cristina A.. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Quintar, Amado Alfredo. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
description Background: 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). Methods: 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. Results: 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. Conclusions: 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.
publishDate 2024
dc.date.none.fl_str_mv 2024-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
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info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/265930
Roldán Gallardo, Franco Fabián; Martínez Piñerez, Daniel E.; Reinarz Torrado, Kevin F.; Berg, Gabriela Alicia; Herzfeld, Jael Dafne; et al.; Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia; MDPI; Biology; 13; 10; 10-2024; 1-15
2079-7737
CONICET Digital
CONICET
url http://hdl.handle.net/11336/265930
identifier_str_mv Roldán Gallardo, Franco Fabián; Martínez Piñerez, Daniel E.; Reinarz Torrado, Kevin F.; Berg, Gabriela Alicia; Herzfeld, Jael Dafne; et al.; Extracellular Vesicles Contribute to Oxidized LDL-Induced Stromal Cell Proliferation in Benign Prostatic Hyperplasia; MDPI; Biology; 13; 10; 10-2024; 1-15
2079-7737
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/doi/10.3390/biology13100827
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eu_rights_str_mv openAccess
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