Change of laminin density stimulates axon branching via growth cone myosin II-mediated adhesion
Change of laminin density stimulates axon branching via growth cone myosin II-mediated adhesion
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DOI：
10.1039/c3ib40131f
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发表时间：
2013-01-01
影响因子：
2.5
通讯作者：
Jiang, Xingyu
中科院分区：
文献类型：
--
作者：
Liu, Wenwen;Xing, Shige;Jiang, Xingyu
轴突分支使神经元能够与多个目标接触并对其微环境做出反应。由于其在神经网络形成中的重要性，轴突分支在过去的几十年中得到了广泛的研究。细胞外基质的化学性质已经被提出来调节轴突的发育，但是它们的密度变化对轴突分支的影响还没有很好的理解。在这里，我们证明了急剧扩大的基板几何形状和层粘连蛋白密度的急剧变化刺激轴突分支，通过使用微接触印刷（μ CP）和微流体印刷（μ FP）技术。我们还发现，层粘连蛋白密度刺激的轴突分支的变化依赖于肌球蛋白II活性。层粘连蛋白密度的变化导致生长锥上丝状伪足的不对称延伸，这是轴突分支的前提条件。这些以前未知的层粘连蛋白密度刺激轴突分支的变化机制可能解释细胞外基质如何调节轴突在体内的分支，并促进体外神经元网络的建立。
Axon branching enables neurons to contact with multiple targets and respond to their microenvironment. Owing to its importance in neuronal network formation, axon branching has been studied extensively during the past decades. The chemical properties of extracellular matrices have been proposed to regulate axonal development, but the effects of their density changes on axon branching are not well understood. Here, we demonstrate that both the sharp broadening of substrate geometry and the sharp change of laminin density stimulate axon branching by using microcontact printing (mu CP) and microfluidic printing (mu FP) techniques. We also found that the change of axon branching stimulated by laminin density depends on myosin II activity. The change of laminin density induces asymmetric extensions of filopodia on the growth cone, which is the precondition for axon branching. These previously unknown mechanisms of change of laminin density-stimulated axon branching may explain how the extracellular matrices regulate axon branching in vivo and facilitate the establishment of neuronal networks in vitro.