TRPM7 and MagT1 regulate the proliferation of osteoblast-like SaOS-2 cells through different mechanisms

Magnes Res. 2020 Feb 1;33(1):12-20. doi: 10.1684/mrh.2020.0463.

Abstract

A correct magnesium (Mg2+) intake is essential for bone health. In particular, Mg2+ deficiency inhibits the proliferation of osteoblast-like SaOS-2 cells by increasing nitric oxide (NO) production through the upregulation of inducible NO synthase. At the moment, little is known about the expression and the role of TRPM7, a channel/enzyme involved in Mg2+ uptake, and MagT1, a Mg2+ selective transporter, in SaOS-2 cells. Here, we demonstrate that TRPM7 is not modulated by different extracellular concentrations of Mg2+ and its silencing exacerbates growth inhibition exerted by low Mg2+ through the activation of inducible NO synthase and consequent accumulation of NO. Moreover, MagT1 is upregulated in SaOS-2 cultured in high Mg2+ and its silencing inhibits the growth of SaOS-2 cultured in media containing physiological or high Mg2+, without any modulation of NO production. We propose that TRPM7 and MagT1 are both involved in regulating SaOS-2 proliferation through different mechanisms.

Keywords: MagT1; Magnesium; TRPM7; bone; osteoblasts.

MeSH terms

  • Cation Transport Proteins / genetics
  • Cation Transport Proteins / metabolism*
  • Cell Proliferation / drug effects
  • Humans
  • Magnesium / pharmacology
  • Nitric Oxide / biosynthesis
  • Osteoblasts*
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • TRPM Cation Channels / genetics
  • TRPM Cation Channels / metabolism*
  • Tumor Cells, Cultured

Substances

  • Cation Transport Proteins
  • MagT1 protein, human
  • TRPM Cation Channels
  • Nitric Oxide
  • Protein Serine-Threonine Kinases
  • TRPM7 protein, human
  • Magnesium