Low doses of Co nanoparticles induce death and regulate osteogenic differentiation in MG-63 cells

Abstract

The aim of the present study was to investigate the effects of cobalt nanoparticles (CoNPs) on the proliferation and differentiation of human osteoblasts in vitro, and to investigate the molecular mechanisms via which CoNPs affect proliferation and differentiation of osteoblasts. The MG‑63 human osteoblast cell line was treated with different concentrations of CoNPs for 12 to 48 h in vitro. At each time point, cell morphology was observed and an MTT assay was performed to assess cell viability. Alkaline phosphatase (ALP), osteocalcin (BGLAP), collagen I (COL I), osteoprotegerin (OPG) and receptor activator of nuclear factor κ‑B ligand mRNA expression levels, and ALP, BGLAP and COL protein expression levels, were assessed by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The viability of MG‑63 cells decreased significantly after treatment with CoNPs. As CoNP concentration increased, a higher growth inhibition and cell death was observed. Compared with CoNPs, treatment with the same concentration of Co2+ may have a greater inhibitory effect on the growth of MG‑63 cells. CoNPs affected the mRNAs expression levels of ALP, BGLAP, COL I and OPG in MG‑63 cells, and reduced the protein expression levels of ALP, BGLAP and COL I. In conclusion, the present study demonstrated that CoNPs induce cytotoxic effects on MG‑63 cells by markedly reducing cell viability and inducing cell death at high concentrations. In addition, CoNPs may inhibit the function and differentiation of osteoblasts by affecting the mRNA and protein expression levels of associated genes. The results of the present study indicate that CoNPs may serve an important role in the aseptic loosening mechanism following total joint replacement surgery, particularly in situations where metal on metal prostheses are used. Further study into inhibiting this effect is required.

Network Pharmacology Integrated Molecular Docking Reveals the Antiosteosarcoma Mechanism of Biochanin A

“…In previous study, expression of BGLAP can be upregulated by the activation of the TP53 and CDKN2A signaling pathway [31]. Han et al have demonstrated that, as a biomarker of bone, the expression of BGLAP was decreased in dying or undifferentiated MG63 cells [32]. In this study, after the treatment of biochanin A, a decreasing trend of BGLAP level can be seen from the western-blot, which may also indicate the death of osteosarcoma cells.…”

Distinct Concentration-Dependent Molecular Pathways Regulate Bone Cell Responses to Cobalt and Chromium Exposure from Joint Replacement Prostheses

“…For cells grown on prosthetic surface, periprosthetic concentrations of 1000 µg/L Co 2+ :Cr 3+ were used. In both cases, the osteoblasts were exposed to the different concentrations of metal ions for 24 h. Previous clinical reports on the levels of circulating and periprothetic Co and Cr has informed the use of these concentrations in this study [ 42 , 43 , 44 , 45 ].…”

<p>Local Cellular Responses to Metallic and Ceramic Nanoparticles from Orthopedic Joint Arthroplasty Implants</p>

“…Further, Co NPs inhibited osteoblastic function and differentiation by affecting mRNA and protein expression levels of genes such as ALP, BGLAP, Col I, OGP, and RANKL . 105 This suggests that Co NPs do not only suppress the osteoblastic growth and differentiation, but also indirectly upregulate osteoclastic function. Similar results have been observed on Saos-2 cells.…”