Extracellular Muscle Myosin II Promotes Sensory Axon Formation.

Extracellular Muscle Myosin II Promotes Sensory Axon Formation.
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DOI:
10.1089/dna.2005.24.438
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发表时间:
2005-07
影响因子:
3.1
通讯作者:
Lee Silver;G. Gallo
Lee Silver;G. Gallo
中科院分区:
生物学4区
文献类型:
--
作者:
Lee Silver;G. Gallo

文献摘要

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肌球蛋白II是一种细胞内产生力的酶,没有已知的细胞外作用。在涉及骨骼肌球蛋白II到胚胎感觉神经元的研磨加载的实验过程中,我们观察到,肌球蛋白II的神经元细胞外应用导致每个神经元发起的轴突数量的稳健增加,但并没有改变轴突延伸的速率。在层粘连蛋白存在下,基质结合肌球蛋白II足以引起轴突形成的增加。然而,在缺乏层粘连蛋白的情况下,细胞外肌球蛋白II单独不足以促进轴突形成,尽管它允许神经营养因子存在下的神经元存活。肌球蛋白II促进附着的神经元的基底层的存在或不存在的层粘连蛋白。除了促进轴突的起始外,细胞外肌球蛋白II还增加了轴突侧支分支的频率。最后,细胞外肌球蛋白II没有影响生长锥崩溃响应semaphorin-IIIA,但衰减硫酸软骨素蛋白多糖对轴突延伸的抑制作用。令人惊讶的是,这些结果表明,细胞外肌球蛋白II促进神经元的附着,并增加轴突的形成和分支。这些观察结果的潜在意义进行了讨论的背景下,肌球蛋白II释放受伤的肌肉和细胞外肌球蛋白II协会与细胞外基质的先前演示。
Myosin II is an intracellular force-generating enzyme with no known extracellular action. In the course of experiments involving trituration loading of skeletal myosin II into embryonic sensory neurons we observed that extracellular application of myosin II to neurons resulted in a robust increase in the number of axons initiated by each neuron, but did not alter the rate of axon extension. Substratum bound myosin II in the presence of laminin was sufficient to elicit increases in axon formation. However, in the absence of laminin, extracellular myosin II alone was not sufficient to promote axon formation, although it allowed neuron survival in the presence of neurotrophin. Myosin II promoted the attachment of neurons to the substratum in the absence or presence of laminin. In addition to promoting the initiation of axons, extracellular myosin II also increased the frequency of axon collateral branching. Finally, extracellular myosin II did not affect growth cone collapse in response to semaphorin-IIIA, but attenuated the inhibitory action of chondroitin sulfate proteoglycans on axon extension. Surprisingly, these results demonstrate that extracellular myosin II promotes attachment of neurons and increases axon formation and branching. The potential significance of these observations is discussed in the context of myosin II release from injured muscle and a previous demonstration of extracellular myosin II association with the extracellular matrix.