Shao Xueying, Sørensen Maja Højvang, Fang Chao, Chang Raymond Chuen Chung, Chu Zhiqin, Lin Yuan
Department of Mechanical Engineering, The University of Hong Kong, Hong Kong, China.
HKU-Shenzhen Institute of Research and Innovation, Shenzhen, China.
Front Bioeng Biotechnol. 2021 Jan 6;8:621777. doi: 10.3389/fbioe.2020.621777. eCollection 2020.
Although it is known that stronger cell-extracellular matrix interactions will be developed as neurons mature, how such change influences their response against traumatic injury remains largely unknown. In this report, by transecting axons with a sharp atomic force microscope tip, we showed that the injury-induced retracting motion of axon can be temporarily arrested by tight NCAM (neural cell adhesion molecule) mediated adhesion patches, leading to a retraction curve decorated with sudden bursts. Interestingly, although the size of adhesion clusters (~0.5-1 μm) was found to be more or less the same in mature and immature neurons (after 7- and 3-days of culturing, respectively), the areal density of such clusters is three times higher in mature axons resulting in a much reduced retraction in response to injury. A physical model was also adopted to explain the observed retraction trajectories which suggested that apparent adhesion energy between axon and the substrate increases from ~0.12 to 0.39 mJ/m as neural cell matures, in good agreement with our experiments.
虽然已知随着神经元成熟会形成更强的细胞-细胞外基质相互作用,但这种变化如何影响它们对创伤性损伤的反应在很大程度上仍不清楚。在本报告中,我们用尖锐的原子力显微镜尖端横切轴突,结果表明轴突损伤诱导的回缩运动可被紧密的神经细胞黏附分子(NCAM)介导的黏附斑暂时阻止,从而产生带有突然爆发的回缩曲线。有趣的是,尽管在成熟和未成熟神经元中(分别培养7天和3天后)发现黏附簇的大小(约0.5 - 1μm)大致相同,但成熟轴突中此类簇的面密度高出三倍,导致损伤后的回缩大大减少。我们还采用了一个物理模型来解释观察到的回缩轨迹,该模型表明随着神经细胞成熟,轴突与底物之间的表观黏附能从约0.12增加到0.39 mJ/m²,这与我们的实验结果高度一致。