Assessment of tantalum nanoparticle-induced MC3T3-E1 proliferation and underlying mechanisms

• Published in: Journal of materials science. Materials in medicine Vol. 32; no. 11; p. 133
• Main Authors: Kang, Chengrong, Wang, Yudong, Li, Liang, Li, Zhangwei, Zhou, Qianbing, Pan, Xuan
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.11.2021; Springer Nature B.V; Springer
• Subjects: 1-Phosphatidylinositol 3-kinase; 3T3 Cells; AKT protein; Animals; Apoptosis; Apoptosis - drug effects; Autophagy; Biocompatibility Studies; Biocompatible Materials; Biomaterials; Biomedical Engineering and Bioengineering; Biomedical materials; Cell cycle; Cell proliferation; Cell Proliferation - drug effects; Cell viability; Ceramics; Chemistry and Materials Science; Cholecystokinin; Chromones - pharmacology; Composites; Electron microscopy; Feedback loops; Flow cytometry; G1 phase; Gene Expression Regulation - drug effects; Glass; Light scattering; Materials Science; Materials Testing; Metal Nanoparticles - chemistry; Metal Nanoparticles - toxicity; Mice; Microscopy; Microtubule-Associated Proteins - genetics; Microtubule-Associated Proteins - metabolism; Morpholines - pharmacology; Nanoparticles; Natural Materials; Phagocytosis; Photon correlation spectroscopy; Polymer Sciences; Pretreatment; Proteins; Rapamycin; Regenerative Medicine/Tissue Engineering; Ribonucleosides - pharmacology; Scanning electron microscopy; Sirolimus - pharmacology; Surfaces and Interfaces; Tantalum; Tantalum - chemistry; Thin Films; TOR protein; Transmission electron microscopy; Western blotting
• ISSN: 0957-4530; 1573-4838
• DOI: 10.1007/s10856-021-06606-7

Objective In our previous study, tantalum nanoparticle (Ta-NPs) was demonstrated to promote osteoblast proliferation via autophagy induction, but the specific mechanism remains unclear. In the present study, we will explore the potential mechanism. Methods Ta-NPs was characterized by transmission electron microscopy, scanning electron microscopy, dynamic light scattering, and BET specific surface area test. MC3T3-E1 were treated with 0 or 20 μg/mL Ta-NPs with or without pretreatment with 10 μM LY294002, Triciribine, Rapamycin (PI3K/Akt/mTOR pathway inhibitors) for 1 h respectively. Western blotting was used to detect the expressions of pathway proteins and LC3B. CCK-8 assay was used to assess cell viability. Flow cytometry was used to detect apoptosis and cell cycle. Results After pretreatment with LY294002, Triciribine and Rapamycin, the p-Akt/Akt ratio of pathway protein in Triciribine and Rapamycin groups decreased ( P  < 0.05), while the autophagy protein LC3-II/LC3-I in the Rapamycin group was upregulated obviously ( P  < 0.001). In all pretreated groups, apoptosis was increased (LY294002 group was the most obvious), G1 phase cell cycle was arrested (Triciribine and Rapamycin groups were more obvious), and MC3T3-E1 cells were proliferated much more ( P  < 0.01, P  < 0.001, P  < 0.05). Conclusion Pretreatment with Triciribine or Rapamycin has a greater effect on pathway protein Akt, cell cycle arrest, autophagy protein, and cell proliferation but with inconsistent magnitude, which may be inferred that the Akt/mTOR pathway, as well as its feedback loop, were more likely involved in these processes.