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Polystyrene microplastics arrest skeletal growth in puberty through accelerating osteoblast senescence
1Department of Orthopedics, Affiliated Hospital of Yangzhou University, Yangzhou, China; Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
Polystyrene microplastics (PS-MPs) accumulate in bones, hindering skeletal growth by promoting osteoblast senescence. Reactivating autophagy may reverse these detrimental effects.
Area of Science:
- Environmental Science
- Toxicology
- Bone Biology
Background:
- Polystyrene microplastics (PS-MPs) are pervasive environmental contaminants.
- Microplastic accumulation in organs can cause toxic effects.
- The skeletal impact of PS-MPs exposure is largely unknown.
Purpose of the Study:
- To investigate the effects of PS-MPs on skeletal development and bone micro-architecture.
- To elucidate the underlying mechanisms of PS-MPs-induced skeletal abnormalities.
- To explore potential therapeutic strategies targeting autophagy.
Main Methods:
- Exposure of mice to PS-MPs.
- Assessment of skeletal growth parameters (body length, bone length).
- Histological and micro-architectural analysis of bone tissues.
- Evaluation of osteoblast number, osteogenic ability, and autophagy markers.
Main Results:
- PS-MPs accumulated in long and axial bones, reducing overall body and bone length.
- Skeletal growth was impaired, with reduced trabecular bone micro-architecture.
- PS-MPs suppressed osteogenic ability by decreasing osteoblast numbers and accelerating osteoblast senescence.
- Impaired autophagy, characterized by reduced autophagosomes and autophagy-related proteins, was observed in senescent osteoblasts.
- Reactivating autophagy reversed osteoblast senescence and ameliorated PS-MPs-induced skeletal growth arrest.
Conclusions:
- PS-MPs detrimentally affect skeletal growth during puberty by accelerating osteoblast senescence.
- Impaired autophagy plays a crucial role in PS-MPs-induced skeletal abnormalities.
- Reactivating autophagy presents a potential therapeutic strategy to counteract PS-MPs' skeletal health threats.
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