Article
Bismuth-based nanoparticles impair adipogenic differentiation of human adipose-derived mesenchymal stem cells
Registro en:
RIBEIRO, Annanda Lyra et al. Bismuth-based nanoparticles impair adipogenic differentiation of human adipose-derived mesenchymal stem cells. Toxicology in Vitro, v. 77, n. 105248, p. 1–10, 2021.
0887-2333
10.1016/j.tiv.2021.105248
Autor
Ribeiro, Annanda Lyra
Bassai, Letícia Werzel
Robert, Anny Waloski
Machado, Thiago Neves
Bezerra Júnior, Arandi Ginane
Horinouchi, Cintia Delai da Silva
Aguiar, Alessandra Melo de
Resumen
Bismuth-based nanoparticles (BiNPs) have attracted attention for their potential biomedical applications.
However, there is a lack of information concerning their interaction with biological systems. In this study, it was
investigated the effect of physically synthesized BiNPs to human adipose-derived stem cells (ADSCs). We first
evaluated the influence of BiNPs on cell viability, cell morphology, mitochondrial function and cell proliferation.
Further, the impact of BiNPs on adipogenic differentiation was also explored. Cytotoxicity assays have demonstrated that BiNPs did not reduce relative cell viability of ADSC except at the highest tested concentration (345 μg/ml). Analysis of cell morphology performed by transmission electron microscopy confirmed that BiNPs induced cell damage only at a high concentration (302.24 μg/ml), equivalent to IC50 concentration. Moreover, BiNPs exposure increased the expression of the cell proliferation marker Ki-67 and the incorporation of the thymidine analogue EdU into cell DNA, suggesting that these nanoparticles could be stimulating ADSC proliferation. BiNPs also increased the mitochondrial membrane potential. Furthermore, BiNPs reduced ADSC adipogenic differentiation as measured by lipid droplet accumulation and mRNA expression levels of the specific adipogenesis biomarkers PPARγ, C/EPBɑ and FABP4. Thus, BiNPs affect the nonspecific (viability, proliferation and mitochondrial activity) and specific (adipogenesis) cellular mechanisms of ADSCs.