Neural mechanobiology and neuronal vulnerability to traumatic loading
Neural mechanobiology and neuronal vulnerability to traumatic loading
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DOI：
10.1016/j.jbiomech.2009.09.011
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发表时间：
2010-01-05
影响因子：
2.4
通讯作者：
Prado, Gustavo R.
中科院分区：
文献类型：
--
作者：
LaPlaca, Michelle C.;Prado, Gustavo R.
为了了解神经元对创伤性损伤的物理耐受性，工程师和神经科学家试图用体外损伤系统与神经系统的分离成分重现创伤事件期间的生物力学环境。这种方法允许人们开始揭示潜在的分子和生化机制，这些机制导致细胞功能障碍和死亡，作为机械输入的功能。过度的机械力和变形导致结构和功能破坏，包括几个关键的有害细胞过程，如膜损伤、钙稳态紊乱、谷氨酸释放、细胞死亡和caspase介导的蛋白质水解。然而，对导致细胞衰竭和功能障碍的机械转导事件的理解还不是很清楚。创伤负荷的机械特征细胞模型对于提高对神经损伤背景下机械转导的理解，改善保护系统，并为测试治疗干预提供受控环境至关重要。本文综述了创伤性神经负荷的细胞力学。我们重点介绍了研究神经元和神经胶质细胞机械阈值的背景和动机，并讨论了一些可能有助于阐明改善耐受性标准和阐明未来研究方向的急性反应。2009爱思唯尔有限公司版权所有。
In order to understand the physical tolerance of neurons to traumatic insults, engineers and neuroscientists have attempted to reproduce the biomechanical environment during a traumatic event using in vitro injury systems with isolated components of the nervous system. This approach allows one to begin to unravel the underlying molecular and biochemical mechanisms that lead to cell dysfunction and death as a function of mechanical inputs. Excess mechanical force and deformation causes structural and functional breakdown, including several key deleterious cellular processes, such as membrane damage, an upset of calcium homeostasis, glutamate release, cell death, and caspase-mediated proteolysis. Understanding of the mechanotransduction events, however, that lead to cellular failure and dysfunction, are not well understood. Mechanically characterized cellular models of traumatic loading are critical to the improved understanding of mechanotransduction in the context of neural injury, the improvement of protective systems, and to provide a controlled setting for testing therapeutic interventions. In this review of the cellular mechanics of traumatic neural loading. we focus on the backdrop and motivation for studying mechanical thresholds in neurons and glial cells and discuss some of the acute responses that may help elucidate improved tolerance criteria and illuminate future research directions. (C) 2009 Elsevier Ltd. All rights reserved.