Zinc Promotes Adipose-Derived Mesenchymal Stem Cell Proliferation and Differentiation towards a Neuronal Fate

Figure 2

Zinc chelation inhibits cellular growth through downregulation of ERK1/2 activity. To investigate whether extracellular zinc chelation affected AD-MSC survival, cultured AD-MSCs were treated with 1 mM CaEDTA in the culture medium. AD-MSC survival was inhibited by the addition of zinc chelators. (a) Phase-contrast photomicrographs of AD-MSCs 6 days after the addition of zinc chelators. Scale bar, 100 μm. (b) The effect of zinc chelators on AD-MSC survival was evaluated using the CCK-8 assay for 6 days. AD-MSCs were pretreated with or without 1 mM CaEDTA and then incubated with ZnCl₂ (30 μM and 100 μM) for 6 days ( versus untreated with ZnCl₂; versus untreated with CaEDTA). (c) To determine whether chelation of zinc affected the activity of ERK, AD-MSCs were treated with or without CaEDTA and then incubated with ZnCl₂ for 24 h. Western blotting using phospho-ERK1/2 and ERK1/2 antibodies was performed. (d) These data represent the mean ± SD from three independent experiments ( versus untreated with ZnCl₂; versus treated with ZnCl₂).

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