Aluminum trichloride inhibits osteoblastic differentiation through inactivation of Wnt/β-catenin signaling pathway in rat osteoblasts

Environ Toxicol Pharmacol. 2016 Mar:42:198-204. doi: 10.1016/j.etap.2015.11.023. Epub 2015 Dec 8.

Abstract

Exposure to aluminum (Al) suppresses bone formation. Osteoblastic differentiation plays a key role in the process of bone formation. However, the effect of Al on osteoblastic differentiation is still controversial, and the mechanism remains unclear. To investigate the effect of Al on osteoblastic differentiation and whether Wnt signaling pathway was involved in it, the primary rat osteoblasts were exposed to 1/40 IC50, 1/20 IC50 and 1/10 IC50 of aluminum trichloride (AlCl3) for 24h, respectively. The activity analysis of alkaline phosphate, qRT-PCR analysis of type I collagen, alkaline phosphate, Wnt3a and Dkk-1, Western blot analysis of p-GSK3β, GSK3β and β-catenin protein and Immunofluorescence staining for β-catenin suggested that AlCl3 inhibited osteoblastic differentiation and Wnt/β-catenin pathway. Moreover, we found exogenous Wnt3a application reversed the inhibitory effect of AlCl3 on osteoblastic differentiation, accompanied by activating the Wnt/β-catenin pathway. Taken together, these findings suggest that AlCl3 inhibites osteoblastic differentiation through inactivation of Wnt/β-catenin pathway in osteoblasts.

Keywords: Aluminum trichloride; Osteoblastic differentiation; Rat osteoblasts; Wnt/β-catenin pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aluminum Chloride
  • Aluminum Compounds / toxicity*
  • Animals
  • Cell Differentiation / drug effects
  • Chlorides / toxicity*
  • Collagen Type I / metabolism
  • Hazardous Substances / toxicity*
  • Osteoblasts / drug effects*
  • Osteogenesis / drug effects
  • Rats
  • Wnt Signaling Pathway / drug effects*

Substances

  • Aluminum Compounds
  • Chlorides
  • Collagen Type I
  • Hazardous Substances
  • Aluminum Chloride