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首页> 外文学位 >An in vitro model for uniaxial stretching of cultured neural cells: The roles of mechanical deformation and Bcl-2 proteins on axonal injury.
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An in vitro model for uniaxial stretching of cultured neural cells: The roles of mechanical deformation and Bcl-2 proteins on axonal injury.

机译：培养的神经细胞单轴拉伸的体外模型：机械变形和Bcl-2蛋白在轴突损伤中的作用。

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摘要

Traumatic brain injury (TBI) is a significant health-care problem in our society and quite often leads to permanent disability or death. Today, over 5.3 million Americans are living with some sort of brain injury related disability (Brain Injury Association). Severe mechanical impact loading as well as non-impact inertial loading to the head may result in large intracranial deformations of the brain tissues and into numerous injuries and biological responses. Macroscopic shear deformation of brain tissue during head injury often translates to a localized stretching of individual neurons and their processes. It is therefore critical to perform uniaxial stretching of the neurons with strains and strain rates that mimic head injury conditions. A unique in vitro injury device has been developed with the capability of stretching cultured neural cells at strains above 100% and strain rates above 100s−1. The effect of strain on the development of axonal injury has been well documented. However, the effect of strain rate on axonal injury has not yet been considered. This study investigates the affects of both strain and strain rate on the death of cultured neurons. Differentiated neurons were uniaxially stretch injured at predetermined strain and strain rates. Our results indicate an equal and possibly a slightly higher strain rate dependence on cell death than strain alone.; Mechanical stretch injury to neural cells has largely been described as a necrotic cell death however, studies now indicate that apoptosis may also be present following TBI. We have investigated whether Bax and BClX L protein overexpression participate in cell death pathways following stretch injury and whether apoptosis is a factor in in vitro models of axonal injury. Bax overexpression produced significant cell death and little neurite development throughout the differentiation of neural precursor cells. Although morphologically correct neural cultures could not be obtained from the YFP-Bax cells, continued experiments did not produce identifiable Bax translocation as a result of stretch injury. Alternatively, BClX L overexpression provided significant protection to neural cells throughout differentiation and in response to a wide range of apoptotic insults in the differentiated state. BClXL overexpression did not however, protect against stretch injury.
机译：脑外伤（TBI）是我们社会中一个重要的医疗保健问题，通常会导致永久性残疾或死亡。如今，有530万美国人患有某种与脑损伤相关的残疾（脑损伤协会）。严重的机械冲击载荷以及对头部的非冲击惯性载荷可能会导致脑组织的颅内大变形，并导致大量伤害和生物学反应。颅脑损伤期间脑组织的宏观剪切变形通常转化为单个神经元及其过程的局部拉伸。因此，至关重要的是对神经元进行单轴拉伸，其应变和应变率应模仿头部受伤状况。已经开发出一种独特的体外损伤装置，该装置具有在超过100％的应变和超过100s -1 的应变速率下拉伸培养的神经细胞的能力。应变对轴突损伤发展的影响已被充分证明。但是，尚未考虑应变率对轴突损伤的影响。这项研究调查了应变和应变率对培养的神经元死亡的影响。分化的神经元在预定的应变和应变率下被单轴拉伸损伤。我们的结果表明，与单独的应变相比，应变率对细胞死亡的依赖性可能更高。对神经细胞的机械拉伸损伤在很大程度上已被描述为坏死细胞死亡，但是，现在的研究表明，TBI后也可能存在凋亡。我们研究了Bax和BClX L 蛋白过表达是否参与牵张性损伤后的细胞死亡途径，并且凋亡是否是体外轴突损伤模型中的一个因素。 Bax过表达在整个神经前体细胞分化过程中产生了明显的细胞死亡和很少的神经突发育。尽管无法从YFP-Bax细胞获得形态学上正确的神经培养物，但由于拉伸损伤，继续进行的实验并未产生可识别的Bax易位。另外，BClX L 的过表达为神经细胞在整个分化过程中提供了显着的保护，并响应分化状态下的各种凋亡。然而，BClX L 的过表达并没有防止拉伸损伤。

著录项

  • 作者

    Pfister, Bryan James.;

  • 作者单位

    The Johns Hopkins University.;

  • 授予单位 The Johns Hopkins University.;
  • 学科 Engineering Biomedical.; Biology Neuroscience.; Chemistry Biochemistry.
  • 学位 Ph.D.
  • 年度 2002
  • 页码 208 p.
  • 总页数 208
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物医学工程;神经科学;生物化学;
  • 关键词

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