The world journal of men's health · 2026
Polystyrene Nanoplastics Induce Penile Endothelial Injury via CLDN1 Downregulation: A Novel Mechanism of Nanoplastic Toxicity.
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Fang Zishui, Niu Fengwen, Gao Pengchao, Zheng Zhongjie, Tan Xiaohui, Xia Mancheng, Li Kefan, Jin Zirun, Zhang Zhe, Guan Ruili, Jiang Hui, Yang Yuzhuo
Аннотация
PURPOSE: Environmental contamination by polystyrene nanoplastics (PS-NPs) has emerged as a growing concern due to their potential adverse effects on human health. Although PS-NPs have been reported to accumulate in penile tissue, their effects on penile endothelial integrity and the underlying mechanisms remain poorly understood. This study aimed to investigate the impact of PS-NPs on penile endothelial injury and to explore the potential molecular mechanisms involved.
MATERIALS AND METHODS: In vivo and in vitro exposure models were established using mixed PS-NPs composed of three particle sizes (25, 50, and 100 nm) in equal proportions. Male mice were exposed to PS-NPs, and penile tissues were evaluated by histological and molecular analyses. In vitro, rat corpus cavernosum endothelial cells (RCCECs) and human umbilical vein endothelial cells (HUVECs) were treated with PS-NPs to assess cell viability, proliferation, transcriptomic alterations, and tight junction-related protein expression.
RESULTS: PS-NPs exposure induced marked structural abnormalities in endothelial cells of the mouse penile vasculature, accompanied by reduced expression of proliferation markers and increased fibrosis in penile tissue. In vitro, PS-NPs significantly decreased RCCEC viability and proliferation in a dose- and time-dependent manner. Transcriptomic analyses revealed enrichment of differentially expressed genes in cell adhesion-related pathways in both mouse penile tissue and RCCECs. Notably, the expression of the tight junction protein Claudin-1 (CLDN1) was significantly downregulated in vivo and in vitro. Furthermore, CLDN1 knockdown reduced endothelial cell viability, whereas CLDN1 overexpression increased endothelial cell viability in both HUVECs and RCCECs.
CONCLUSIONS: These findings indicate that PS-NPs exposure induces penile endothelial injury and fibrosis, potentially through disruption of cell adhesion and tight junction integrity mediated by CLDN1 downregulation, providing mechanistic insight into the potential risks of PS-NPs exposure to male sexual health.
MATERIALS AND METHODS: In vivo and in vitro exposure models were established using mixed PS-NPs composed of three particle sizes (25, 50, and 100 nm) in equal proportions. Male mice were exposed to PS-NPs, and penile tissues were evaluated by histological and molecular analyses. In vitro, rat corpus cavernosum endothelial cells (RCCECs) and human umbilical vein endothelial cells (HUVECs) were treated with PS-NPs to assess cell viability, proliferation, transcriptomic alterations, and tight junction-related protein expression.
RESULTS: PS-NPs exposure induced marked structural abnormalities in endothelial cells of the mouse penile vasculature, accompanied by reduced expression of proliferation markers and increased fibrosis in penile tissue. In vitro, PS-NPs significantly decreased RCCEC viability and proliferation in a dose- and time-dependent manner. Transcriptomic analyses revealed enrichment of differentially expressed genes in cell adhesion-related pathways in both mouse penile tissue and RCCECs. Notably, the expression of the tight junction protein Claudin-1 (CLDN1) was significantly downregulated in vivo and in vitro. Furthermore, CLDN1 knockdown reduced endothelial cell viability, whereas CLDN1 overexpression increased endothelial cell viability in both HUVECs and RCCECs.
CONCLUSIONS: These findings indicate that PS-NPs exposure induces penile endothelial injury and fibrosis, potentially through disruption of cell adhesion and tight junction integrity mediated by CLDN1 downregulation, providing mechanistic insight into the potential risks of PS-NPs exposure to male sexual health.