Journal
ENVIRONMENTAL POLLUTION
Volume 311, Issue -, Pages -Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.envpol.2022.119963
Keywords
Polystyrene microplastics; Myocardial developmental disorders; Endoplasmic reticulum stress; Autophagy; Birds
Categories
Funding
- Natural Science Foundation of Hei- longjiang Province of China [ZD2020C005]
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In complex ecosystems, birds serve as good bioindicators for monitoring environmental contaminants due to their long lifespan and high trophic positions. However, the effects of microplastics (MPs) on myocardial development in birds remain unknown. This study established an in vivo model of chicks exposed to polystyrene microplastics (PS-MPs) and an in vitro model using chicken embryos to explore the molecular mechanisms underlying the impact of PS-MPs on bird myocardial development. The results showed that PS-MPs induced myocardial dysplasia in birds through the ER stress-mediated autophagic pathway. This research provides valuable data for protecting birds from the health risks of MPs pollution and offers insights into addressing the issue of MPs pollution in complex ecosystems.
In complex ecosystems, birds are generally long-lived and occupy high trophic positions, making them good bioindicators for monitoring environmental contaminants. The effects of microplastics (MPs) on myocardial development in bird is currently unknown. Chicks, as a high trophic level terrestrial bird, may be more affected by MPs exposure and. Therefore, we established an in vivo model of chicks exposed to different concentrations of polystyrene microplastics (PS-MPs) and selected 12-day-old chicken embryos in vitro to extract primary car-diomyocytes to further investigate the potential molecular mechanisms of the effect of PS-MPs on myocardial development in birds. Histopathological observations revealed that the PS-MPs treated exhibited loose and irregular myocardial arrangement, large cell gaps and broken myocardial fiber bundles. More mechanistically, TnnT2, Nkx2-5, Gata4, TBX5 and ACTN2 were down-regulated, endoplasmic reticulum (ER) stress markers GRP78, PERK, eIF2 alpha, IRE1, ATF4, ATF6 and CHOP were overexpressed, autophagy-related genes LC3, ATG5, Beclin1 and P62 were down-expressed after PS-MPs exposure, and the addition of 4PBA effectively deregulated the above aberrant expression. Hence, our report indicated that PS-MPs induced myocardial dysplasia in birds is mainly attributed to the ER stress-mediated autophagic pathway. This provided data supporting the protection of birds from the health risks of MPs pollution. More critically, the study of cardiac developmental toxicity in birds may help to better explain or solve the problem of MPs pollution in complex ecosystems.
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