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细胞外囊泡促进氧化型低密度脂蛋白诱导的良性前列腺增生基质细胞增殖。

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

作者信息

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

机构信息

Centro de Microscopía Electrónica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba 5000, Argentina.

Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Córdoba 5000, Argentina.

出版信息

Biology (Basel). 2024 Oct 16;13(10):827. doi: 10.3390/biology13100827.

DOI:10.3390/biology13100827
PMID:39452137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11504470/
Abstract

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.

摘要

背景

临床和实验证据已将良性前列腺增生（BPH）与血脂异常和高胆固醇血症联系起来，但其潜在的细胞机制仍不清楚。本研究调查血脂异常，特别是氧化型低密度脂蛋白（OxLDL），对前列腺基质细胞增殖和细胞外囊泡（EVs）释放的影响。

方法

给小鼠喂食高脂饮食，并用OxLDL处理人前列腺基质细胞（HPSCs）。进行增殖测定和EV表征，以评估EVs在BPH进展中的作用。

结果

促动脉粥样硬化状态显著增加了小鼠前列腺细胞和HPSCs的细胞增殖。用二甲双胍治疗可有效抑制OxLDL诱导的增殖。此外，OxLDL刺激HPSCs产生和释放促增殖EVs，进一步促进细胞增殖。

结论

研究结果表明，血脂异常驱动前列腺基质细胞增殖和EV分泌，促进BPH进展。二甲双胍显示出作为减轻这些影响的治疗药物的潜力，为BPH管理的新策略提供了见解。本研究强调了在BPH发病机制背景下血脂异常、细胞增殖和细胞外通讯之间的复杂相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/af9ae2b638b7/biology-13-00827-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/5ac0b5c8721a/biology-13-00827-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/1ea2d18883f2/biology-13-00827-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/086d0e0c9d46/biology-13-00827-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/eb1f9fb4c5c2/biology-13-00827-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/af9ae2b638b7/biology-13-00827-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/5ac0b5c8721a/biology-13-00827-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/1ea2d18883f2/biology-13-00827-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/086d0e0c9d46/biology-13-00827-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/eb1f9fb4c5c2/biology-13-00827-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b406/11504470/af9ae2b638b7/biology-13-00827-g005.jpg

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