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TRPM7 和 MagT1 通过不同的机制调节成骨样 SaOS-2 细胞的增殖。

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

机构信息

Dipartimento di Scienze Biomediche e Cliniche L. Sacco, Università di Milano, Milano I-20157, Italy.

出版信息

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

Abstract

A correct magnesium (Mg) intake is essential for bone health. In particular, Mg 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 Mg uptake, and MagT1, a Mg selective transporter, in SaOS-2 cells. Here, we demonstrate that TRPM7 is not modulated by different extracellular concentrations of Mg and its silencing exacerbates growth inhibition exerted by low Mg through the activation of inducible NO synthase and consequent accumulation of NO. Moreover, MagT1 is upregulated in SaOS-2 cultured in high Mg and its silencing inhibits the growth of SaOS-2 cultured in media containing physiological or high Mg, without any modulation of NO production. We propose that TRPM7 and MagT1 are both involved in regulating SaOS-2 proliferation through different mechanisms.

摘要

正确的镁 (Mg) 摄入对骨骼健康至关重要。特别是,Mg 缺乏通过上调诱导型一氧化氮合酶增加一氧化氮 (NO) 产生来抑制成骨样 SaOS-2 细胞的增殖。目前,关于参与 Mg 摄取的通道/酶 TRPM7 和 Mg 选择性转运体 MagT1 在 SaOS-2 细胞中的表达和作用知之甚少。在这里,我们证明 TRPM7 不受不同细胞外 Mg 浓度的调节,其沉默通过诱导型一氧化氮合酶的激活和随后的 NO 积累加剧低 Mg 引起的生长抑制。此外,在高 Mg 中培养的 SaOS-2 中上调 MagT1,其沉默抑制含有生理或高 Mg 的培养基中 SaOS-2 的生长,而不调节 NO 产生。我们提出 TRPM7 和 MagT1 都通过不同的机制参与调节 SaOS-2 的增殖。

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