Vitamin D protects against immobilization-induced muscle atrophy via neural crest-derived cells in mice
Vitamin D protects against immobilization-induced muscle atrophy via neural crest-derived cells in mice
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DOI：
10.1038/s41598-020-69021-y
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发表时间：
2020-07-22
影响因子：
4.6
通讯作者：
Miyamoto, Takeshi
中科院分区：
文献类型：
--
作者：
Nakamura, Satoshi;Sato, Yuiko;Miyamoto, Takeshi
维生素D缺乏是公认的石棺减少症的危险因素，但其发生机制尚不清楚。在这里，我们表明，低维生素D状态恶化了制动诱导的小鼠肌肉萎缩。缺乏维生素D受体(VDR)的小鼠在肢体制动后表现出比对照组更严重的肌肉萎缩。此外，与骨骼肌特异的VDR缺陷小鼠相比，神经脊特异性小鼠的制动所致的肌肉萎缩更严重。与对照组相比，VDR缺陷小鼠固定肌肉中的肿瘤坏死因子α的表达显著增加，并且在神经脊特异性而不是肌肉特异性的VDR缺陷小鼠中显著升高。此外，在缺乏肿瘤坏死因子α的小鼠中，由肢体制动引起的肌肉萎缩在低维生素D小鼠中得到显著抑制。我们得出结论，维生素D通过在神经脊来源的细胞中表达VDR来拮抗制动诱导的肌肉萎缩。
Vitamin D deficiency is a recognized risk factor for sarcopenia development, but mechanisms underlying this outcome are unclear. Here, we show that low vitamin D status worsens immobilization-induced muscle atrophy in mice. Mice globally lacking vitamin D receptor (VDR) exhibited more severe muscle atrophy following limb immobilization than controls. Moreover, immobilization-induced muscle atrophy was worse in neural crest-specific than in skeletal muscle-specific VDR-deficient mice. Tnf alpha expression was significantly higher in immobilized muscle of VDR-deficient relative to control mice, and was significantly elevated in neural crest-specific but not muscle-specific VDR-deficient mice. Furthermore, muscle atrophy induced by limb immobilization in low vitamin D mice was significantly inhibited in Tnf alpha -deficient mice. We conclude that vitamin D antagonizes immobilization-induced muscle atrophy via VDR expressed in neural crest-derived cells.