Mechanoporation is a potential indicator of tissue strain and subsequent degeneration following experimental traumatic brain injury
Mechanoporation is a potential indicator of tissue strain and subsequent degeneration following experimental traumatic brain injury
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DOI：
10.1016/j.clinbiomech.2018.05.016
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发表时间：
2019-04-01
影响因子：
1.8
通讯作者：
Zhang, Liying
中科院分区：
文献类型：
--
作者：
LaPlaca, Michelle C.;Lessing, M. Christian;Zhang, Liying
背景资料：质膜渗透性的增加是创伤性脑损伤急性病理学的一部分，并且可能是过度膜力的函数。这种膜损伤或机械穿孔允许离子和其他分子穿过质膜的非特异性通量，并可能最终导致细胞死亡。然而，组织应力和应变、膜渗透性和随后的细胞变性之间的关系尚不完全清楚。方法：在损伤前将不同大小的荧光分子引入脑脊液间隙，并在损伤后10 min或24 h处死动物。我们比较了空间分布的质膜损伤后控制皮质的影响在大鼠的应力和应变组织模式在3-D有限元模拟的损伤parameters.Findings：渗透性细胞主要位于同侧皮质和海马损伤大鼠在10分钟后损伤，但24小时也有一个显着增加的渗透性细胞的数量。渗透性标记物摄取和Fluorojade染色的共定位分析揭示了在24 h时具有变性迹象的渗透性细胞的子集，但在绝大多数变性细胞中质膜损伤是明显的。通过有限元模型估计的最大主应变和剪切应力的区域和次区域分布模式与压缩冲击后的细胞膜损伤概况相当。这些结果表明，急性膜渗透性是突出的创伤性脑损伤后，在地区，经历高剪切或拉伸应力和应变，由于不同的机械性能的细胞和组织这种机械穿孔可能在继发性损伤的起始中起作用，导致细胞死亡。
Background: An increases in plasma membrane permeability is part of the acute pathology of traumatic brain injury and may be a function of excessive membrane force. This membrane damage, or mechanoporation, allows non-specific flux of ions and other molecules across the plasma membrane, and may ultimately lead to cell death. The relationships among tissue stress and strain, membrane permeability, and subsequent cell degeneration, however, are not fully understood.Methods: Fluorescent molecules of different sizes were introduced to the cerebrospinal fluid space prior to injury and animals were sacrificed at either 10 min or 24 h after injury. We compared the spatial distribution of plasma membrane damage following controlled cortical impact in the rat to the stress and strain tissue patterns in a 3-D finite element simulation of the injury parameters.Findings: Permeable cells were located primarily in the ipsilateral cortex and hippocampus of injured rats at 10 min post-injury; however by 24 h there was also a significant increase in the number of permeable cells. Analysis of colocalization of permeability marker uptake and Fluorojade staining revealed a subset of permeable cells with signs of degeneration at 24 h, but plasma membrane damage was evident in the vast majority of degenerating cells. The regional and subregional distribution patterns of the maximum principal strain and shear stress estimated by the finite element model were comparable to the cell membrane damage profiles following a compressive impact.Interpretation: These results indicate that acute membrane permeability is prominent following traumatic brain injury in areas that experience high shear or tensile stress and strain due to differential mechanical properties of the cell and tissue organization, and that this mechanoporation may play a role in the initiation of secondary injury, contributing to cell death.