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Nanoplastic impact on bone microenvironment: A snapshot from murine bone cells.
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Researchers investigated how nanoplastics affect the bone microenvironment using murine bone cell models, examining effects on osteoblast and osteoclast activity that regulate bone formation and resorption. Nanoplastic exposure disrupted bone cell function, raising concerns about skeletal health impacts from daily plastic particle exposure.
We live in a plastic world: every day, a wide array of plastics of different compositions, shapes, and sizes contaminate the environment and enter the food chain, profoundly affecting our lives and human health. Nanoplastics (NPs) are emerging as one of our time's most important environmental pollutants to which human organisms are exposed due to their capability to cross cell membranes and induce cellular toxicity. Recent studies reported that NPs toxic effect is partially mediated by oxidative stress (OS). Reactive oxygen species (ROS) are among the most critical factors involved in disrupting skeleton integrity and promoting bone resorption. This study aimed to investigate the impact of OS derived from NP exposure on bone microenvironment. We treated murine bone cells (MC3T3-E1 pre-osteoblast, MLOY-4 osteocyte-like cells, and RAW264.7 pre-osteoclast) with NPs at different concentrations. We found that NPs, once internalized, affect cell viability (assessed by MTT assay), induce ROS production (evaluated by DCFHDA assay), and trigger caspase 3/7 mediated apoptosis (assessed by a fluorometric assay) in all the cell lines tested. NPs hamper the pre-osteoblasts migration capability and potentiate the osteoclastogenesis in pre-osteoclasts by increasing their differentiation toward osteoclasts. We also performed a transcriptomic analysis evaluating gene expression in bone remodeling. Our results showed that OS by NPs induces in RAW264.7 cells an increased expression of genes related to the osteoclastogenic commitment of pre-osteoclasts, together with a disruption of the genes involved in osteoblastogenesis and modulation of inflammatory pathway-related genes in MC3T3-E1 and MLOY-4 cells, respectively. A better understanding of the impact of NPs on bone cell activities resulting in vivo in impaired bone turnover could give more information on the toxicity consequence of NPs on bone mass and the subsequent public health problems, such as bone disease. Also see: https://micro2024.sciencesconf.org/559009/document
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