We live in a plastic world. Plastic waste deeply affects not only our environment but also our health entering the food chain. Only a few studies tested nanoplastic (NP) effects on human health. NP toxic actions are, in part, mediated by oxidative stress (OS) that, among its effects, can influence bone remodeling and epigenome. Epigenetic regulation mechanisms mediate the genome response to environmental stimuli. My hypothesis is: “Could NPs influence skeleton remodeling through OS?”. I have tested my hypothesis on bone physiological environments to take a full-resolution picture. Murine bone cell cultures (MC3T3-E1 preosteoblasts, MLOY4 osteocyte-like cells, and RAW264.7 pre-osteoclasts) were used to test the NPs detrimental effects. The above cells were treated with increasing NPs concentrations (polystyrene NPs, diameter 50 nm, ranging from 0.1 to 200 ug/ml, exposure from 24 to 72 hours) and tested for cell viability (by MTT assay), ROS level (by DCF) and apoptosis (fluorimetric assay). Cellular morphology and NPs localization were also assessed. We have analyzed the migration capability of MC3T3-E1 cells. Lastly, we have analyzed the transcriptomic profile of MC3T3-E1 and MLOY4 cells. NPs (from 100 ug/ml, 48 hours exposure) affect cell viability and induce ROS production (both oxygen and nitrogen reactive species) in all cells lines considered. NPs induce apoptosis (by the activation of caspase 3/7) both in preosteoblasts and pre-osteoclasts. NPs affect the preosteoblasts migration capability, directly involved in bone remodeling. We found that NPs affect the expression of genes related to inflammatory and osteogenic pathways. In preosteoblasts and osteocytes, NPs reduce the gene expression of HSD11b1, involved in glucocorticoid metabolism. We are now investigating the epigenome contribution of NP detrimental effects in bone cells. The environmental impact of NPs is an increasingly worrying problem for human health due to the large-scale growth of plastic production and its resistance to degradation. 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 possible toxicity consequence of NPs on bone mass and the subsequent health problems, such as bone disease.
Nanoplastics & health: taking a picture of bone cells / L. Casati, D. Giannandrea, V. Citro, N. Platonova, M. Sugni Daniele Bottai, M. Parolini, R. Chiaramonte. ((Intervento presentato al convegno SIPMeT Young Scientist Meeting. MOLECULAR PATHOLOGY: FROM BENCH TO BEDSIDE : December, 10 - 11 tenutosi a Perugia nel 2021.
Nanoplastics & health: taking a picture of bone cells
L. Casati
;D. Giannandrea;V. Citro;N. Platonova;M. Parolini;R. Chiaramonte
2021
Abstract
We live in a plastic world. Plastic waste deeply affects not only our environment but also our health entering the food chain. Only a few studies tested nanoplastic (NP) effects on human health. NP toxic actions are, in part, mediated by oxidative stress (OS) that, among its effects, can influence bone remodeling and epigenome. Epigenetic regulation mechanisms mediate the genome response to environmental stimuli. My hypothesis is: “Could NPs influence skeleton remodeling through OS?”. I have tested my hypothesis on bone physiological environments to take a full-resolution picture. Murine bone cell cultures (MC3T3-E1 preosteoblasts, MLOY4 osteocyte-like cells, and RAW264.7 pre-osteoclasts) were used to test the NPs detrimental effects. The above cells were treated with increasing NPs concentrations (polystyrene NPs, diameter 50 nm, ranging from 0.1 to 200 ug/ml, exposure from 24 to 72 hours) and tested for cell viability (by MTT assay), ROS level (by DCF) and apoptosis (fluorimetric assay). Cellular morphology and NPs localization were also assessed. We have analyzed the migration capability of MC3T3-E1 cells. Lastly, we have analyzed the transcriptomic profile of MC3T3-E1 and MLOY4 cells. NPs (from 100 ug/ml, 48 hours exposure) affect cell viability and induce ROS production (both oxygen and nitrogen reactive species) in all cells lines considered. NPs induce apoptosis (by the activation of caspase 3/7) both in preosteoblasts and pre-osteoclasts. NPs affect the preosteoblasts migration capability, directly involved in bone remodeling. We found that NPs affect the expression of genes related to inflammatory and osteogenic pathways. In preosteoblasts and osteocytes, NPs reduce the gene expression of HSD11b1, involved in glucocorticoid metabolism. We are now investigating the epigenome contribution of NP detrimental effects in bone cells. The environmental impact of NPs is an increasingly worrying problem for human health due to the large-scale growth of plastic production and its resistance to degradation. 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 possible toxicity consequence of NPs on bone mass and the subsequent health problems, such as bone disease.File | Dimensione | Formato | |
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