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Unraveling the impact of nanoplastics on bone microenvironment: focus on extracellular vesicle-mediated communication and oxidative stress in multiple myeloma.
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Researchers reviewed how nanoplastics affect the bone microenvironment, focusing on oxidative stress pathways and extracellular matrix disruption as key mechanisms of toxicity. Reactive oxygen species generated by nanoplastic exposure were identified as drivers of bone cell damage.
Nanoplastics (NPs) have emerged as a novel, worrisome issue in environmental and human well-being studies due to their capability to cross cell membranes and induce cellular toxicity. Recent studies reported that NPs toxic effect is mediated by oxidative stress (OS). Reactive oxygen species (ROS) are among the most critical factors disrupting skeleton integrity and promoting bone resorption. Thus, NPs, once penetrated into the bone, exert a detrimental effect on bone, both in native and in pathologic conditions such as multiple myeloma (MM). MM is a hematological malignancy that finds a willing tumoral niche in the bone. The initial bone disruption affects mesenchymal/osteoblast and osteoclast differentiation, promoting MM development. The bone microenvironment is highly fine-tuned, and extracellular vesicles (EVs) play a crucial role; by transferring their specific functional molecular cargo, NPs could represent a new OS source affecting the bone microenvironment and MM biology. This work aims to unravel the role of OS induced by NPs exposure in educating bone microenvironment through MM-derived EVs intercellular communication. We found that NPs, once uptaken in a dose-dependent way by stromal and MM cells, induce a reduction of cell viability and proliferation correlated to ROS production. Nanoparticle tracking analysis and a flow cytometry analysis show that EVs derived from MM cells NPs-exposed show a reduced diameter and higher concentration of nanoparticles.We also observed that education of preosteoblast with NPs-MM-EVs restores the correct level of the osteoblastogenic factor Runx2. This reduction could be transmitted by EVs controlling miR505, which is involved in osteoblastogenesis. We observed a decrease in the miR505 level in MM cells exposed, potentially related to a reduction of miR505 in EVs cargo and a slight change in H3K4me3 content. This work could open new insights into MM etiopathogenesis and treatment, especially for the MM side effects of osteolytic lesions. Also see: https://micro2024.sciencesconf.org/558731/document
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