Prostatic fluid exosome-mediated microRNA-155 promotes the pathogenesis of type IIIA chronic prostatitis

前列腺液外泌体介导的microRNA-155促进IIIA型慢性前列腺炎的发病机制

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作者:Baixiong Zhao, Jun Zheng, Yang Qiao, Yongquan Wang, Yang Luo, Dinglin Zhang, Qiyan Cai, Yang Xu, Zhansong Zhou, Wenhao Shen

Background

The latest research has shown that exosomes play an important role in cell-to-cell communication and are closely related to the occurrence of many chronic inflammatory diseases. However, no studies have clarified whether exosomes are involved in the pathogenesis of aseptic inflammation, type IIIA chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS-A). This study aimed to explore the relationship between prostatic fluid exosomes and CP/CPPS-A and reveal new pathogenesis.

Conclusions

Exosomes in the prostatic fluid and the miRNA-155 contained therein were may be involved with the pathogenesis of CP/CPPS-A.

Methods

Our group collected prostatic fluid samples from CP/CPPS-A patients and normal adult men. Electron microscope, quantitative PCR (qPCR), Western Blot, nanoparticle tracking analysis, hematoxylin-and-eosin (HE) staining, immunofluorescence staining and miRNA-155 functional analysis were used to verify the role of exosomes in CP/CPPS-A in vivo and in vitro.

Results

Exosomes were abundantly enriched in the prostatic fluid of CP/CPPS-A patients and selectively overloaded with microRNA-155 (miRNA-155). These exosomes were taken up by prostatic stromal cells in large quantities. They activated interleukin (IL)-8 and tumor necrosis factor-alpha (TNF-α) expression in vitro, and the integrity of the exosomes' plasma membrane is a necessary condition for information transmission by exosomes. In in vivo experiments, histological results showed that prostatic fluid exosomes induced prostatitis in rats. Also, immunofluorescence staining showed excessive activation of IL-8, TNF-α, and inducible nitric oxide synthase (iNOS). Conclusions: Exosomes in the prostatic fluid and the miRNA-155 contained therein were may be involved with the pathogenesis of CP/CPPS-A.

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