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MRF4在受神经支配的成年骨骼肌中的选择性作用:MRF4基因敲除小鼠中Na(V) 1.4钠离子通道表达降低。

A selective role for MRF4 in innervated adult skeletal muscle: Na(V) 1.4 Na+ channel expression is reduced in MRF4-null mice.

作者信息

Thompson Amy L, Filatov Gregory, Chen Connie, Porter Isaac, Li Yingjie, Rich Mark M, Kraner Susan D

机构信息

Department of Molecular and Biomedical Pharmacology, University of Kentucky Medical Center, Lexington, KY 40536, USA.

出版信息

Gene Expr. 2005;12(4-6):289-303. doi: 10.3727/000000005783992034.

Abstract

The factors that regulate transcription and spatial expression of the adult skeletal muscle Na+ channel, Na(V) 1.4, are poorly understood. Here we tested the role of the transcription factor MRF4, one of four basic helix-loop-helix (bHLH) factors expressed in skeletal muscle, in regulation of the Na(V) 1.4 Na+ channel. Overexpression of MRF4 in C2C12 muscle cells dramatically elevated Na(V) 1.4 reporter gene expression, indicating that MRF4 is more efficacious than the other bHLH factors expressed at high levels endogenously in these cells. In vivo, MRF4 protein was found both in extrajunctional and subsynaptic muscle nuclei. To test the importance of MRF4 in Na(V) 1.4 gene regulation in vivo, we examined Na+ channel expression in MRF4-null mice using several techniques, including Western blotting, immunocytochemistry, and electrophysiological recording. By all methods, we found that expression of the Na(V) 1.4 Na+ channel was substantially reduced in MRF4-null mice, both in the surface membrane and at neuromuscular junctions. In contrast, expression of the acetylcholine receptor, and in particular its alpha subunit, was unchanged, indicating that MRF4 regulation of Na+ channel expression was selective. Expression of the bHLH factors myf-5, MyoD, and myogenin was increased in MRF4-null mice, but these factors were not able to fully maintain Na(V) 1.4 Na+ channel expression either in the extrajunctional membrane or at the synapse. Thus, MRF4 appears to play a novel and selective role in adult muscle.

摘要

调节成年骨骼肌钠通道Na(V) 1.4转录和空间表达的因素目前还知之甚少。在此,我们测试了转录因子MRF4(在骨骼肌中表达的四种基本螺旋-环-螺旋(bHLH)因子之一)在调节Na(V) 1.4钠通道中的作用。MRF4在C2C12肌肉细胞中的过表达显著提高了Na(V) 1.4报告基因的表达,这表明MRF4比这些细胞中内源性高水平表达的其他bHLH因子更有效。在体内,MRF4蛋白在肌膜外和突触下肌核中均有发现。为了测试MRF4在体内对Na(V) 1.4基因调控的重要性,我们使用了多种技术,包括蛋白质免疫印迹法、免疫细胞化学法和电生理记录法,来检测MRF4基因敲除小鼠中的钠通道表达。通过所有这些方法,我们发现,在MRF4基因敲除小鼠中,Na(V) 1.4钠通道在表面膜和神经肌肉接头处的表达均大幅降低。相比之下,乙酰胆碱受体,尤其是其α亚基的表达没有变化,这表明MRF4对钠通道表达的调控具有选择性。bHLH因子myf-5、MyoD和肌细胞生成素在MRF4基因敲除小鼠中的表达增加,但这些因子在肌膜外或突触处均无法完全维持Na(V) 1.4钠通道的表达。因此,MRF4似乎在成年肌肉中发挥着一种新的选择性作用。

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本文引用的文献

1
Accumulation of Nav1 mRNAs at differentiating postsynaptic sites in rat soleus muscles.
Mol Cell Neurosci. 2005 Apr;28(4):694-702. doi: 10.1016/j.mcn.2004.11.015.
2
Activity-dependent presynaptic regulation of quantal size at the mammalian neuromuscular junction in vivo.
J Neurosci. 2005 Jan 12;25(2):343-51. doi: 10.1523/JNEUROSCI.3252-04.2005.
3
Mrf4 determines skeletal muscle identity in Myf5:Myod double-mutant mice.
Nature. 2004 Sep 23;431(7007):466-71. doi: 10.1038/nature02876.
4
Hyperpolarized shifts in the voltage dependence of fast inactivation of Nav1.4 and Nav1.5 in a rat model of critical illness myopathy.
J Physiol. 2004 Sep 15;559(Pt 3):813-20. doi: 10.1113/jphysiol.2004.062349. Epub 2004 Jul 14.
6
Aberrant development of motor axons and neuromuscular synapses in MyoD-null mice.
J Neurosci. 2003 Jun 15;23(12):5161-9. doi: 10.1523/JNEUROSCI.23-12-05161.2003.
7
Specific activation of the acetylcholine receptor subunit genes by MyoD family proteins.
J Biol Chem. 2003 Aug 29;278(35):33169-74. doi: 10.1074/jbc.M304744200. Epub 2003 Jun 14.
10
Crucial role of sodium channel fast inactivation in muscle fibre inexcitability in a rat model of critical illness myopathy.
J Physiol. 2003 Mar 1;547(Pt 2):555-66. doi: 10.1113/jphysiol.2002.035188. Epub 2003 Jan 24.

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