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Published on: January 13, 2012
PET-microplastics trigger endothelial glycocalyx loss via ER stress and ROS unleashing IL-1β-driven SMC switching and
Weixue Huo1, Jin Qu1, Sen Wang1
1Department of Vascular Surgery, Intervention Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, People's Republic of China.
Abstract:
Polyethylene terephthalate microplastics (PET-MPs), a major microplastics component identified in human vasculature, pose emerging environmental health risks. This study systemically profiled MPs in human aortic tissues and investigated the mechanisms underlying PET-MPs-induced aortic injury in vivo and in vitro. Chronic oral exposure of Sprague-Dawley rats to PET-MPs resulted in endothelial glycocalyx loss and structural impairment of aortic elastic fibers. Transcriptomic and proteomic analyses elucidated that PET-MPs triggered endoplasmic reticulum stress and reactive oxygen species generation, initiating glycocalyx loss and inflammatory activation. This response further pinpointed interleukin-1β (IL-1β) as a pivotal mediator inducing smooth muscle cell phenotypic switching. Crucially, restoration of the glycocalyx using sulodexide mitigated endothelial dysfunction and downstream smooth muscle cells phenotypic switching. These findings establish endothelial glycocalyx degradation via endoplasmic reticulum stress-reactive oxygen species as a novel mechanism for PET-MPs-induced vascular injury and highlight glycocalyx protection as a potential strategy against environmental microplastic hazards.
Insights
Polyethylene terephthalate microplastics (PET-MPs) cause aortic injury by damaging the endothelial glycocalyx, leading to vascular damage. Protecting the glycocalyx may prevent microplastic-induced health risks.
Area of Science:
- Environmental Health
- Toxicology
- Cardiovascular Science
Background:
- Polyethylene terephthalate microplastics (PET-MPs) are increasingly found in human vasculature.
- Their presence poses potential environmental health risks, particularly to the cardiovascular system.
Purpose of the Study:
- To investigate the mechanisms of PET-MPs-induced aortic injury.
- To profile microplastics in human aortic tissues and assess their impact in vivo and in vitro.
Main Methods:
- Chronic oral exposure of rats to PET-MPs.
- Analysis of aortic tissues for endothelial glycocalyx and elastic fibers.
- Transcriptomic and proteomic analyses to identify molecular pathways.
- In vitro studies to confirm mechanisms and test interventions.
Main Results:
- PET-MPs exposure led to endothelial glycocalyx loss and aortic elastic fiber damage.
- Mechanisms involved endoplasmic reticulum stress and reactive oxygen species generation.
- Interleukin-1β (IL-1β) was identified as a key mediator in smooth muscle cell changes.
- Sulodexide treatment restored the glycocalyx, mitigating endothelial dysfunction.
Conclusions:
- Endothelial glycocalyx degradation is a novel mechanism for PET-MPs-induced vascular injury.
- PET-MPs trigger ER stress and ROS, leading to inflammation and vascular damage.
- Glycocalyx protection presents a potential strategy against microplastic-related vascular hazards.
