Autophagy Protects MC3T3-E1 Cells upon Aluminum-Induced Apoptosis.

Publisher: Humana Press Country of Publication: United States NLM ID: 7911509 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1559-0720 (Electronic) Linking ISSN: 01634984 NLM ISO Abbreviation: Biol Trace Elem Res Subsets: MEDLINE

Original Publication: [London, Clifton, N. J.] Humana Press.

Aluminum Chloride/*pharmacology ; Apoptosis/*drug effects ; Autophagy/*physiology; 3T3 Cells ; Animals ; Cell Survival/drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Mice

Aluminum (Al) exposure has adverse effects on osteoblasts, and the effect might be through autophagy-associated apoptosis. In this study, we showed that aluminum trichloride (AlCl 3 ) could induce autophagy in MC3T3-E1 cells, as demonstrated by monodansylcadaverine (MDC) staining and the expressions of the ATG3, ATG5, and ATG9 genes. We found AlCl 3 inhibited MC3T3-E1 cell survival rate and caused apoptosis, as evidenced by CCK-8 assay, Annexin V/PI double staining, and increased expressions of Bcl-2, Bax, and Caspase-3 genes. In addition, increased autophagy induced by rapamycin further attenuated the MC3T3-E1 cell apoptosis rate after AlCl 3 exposure. These results support the hypothesis that autophagy plays a protective role in impeding apoptosis caused by AlCl 3 . Activating autophagy may be a strategy for treatment of Al-induced bone disease.

31372496 National Natural Science Foundation of China

Keywords: Aluminum; Apoptosis; Autophagy; MC3T3-E1 cell

3CYT62D3GA (Aluminum Chloride)

Date Created: 20180310 Date Completed: 20181220 Latest Revision: 20181220

20240829

10.1007/s12011-018-1264-7

29520724