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Endothelial cell apoptosis in high wall shear stress and wall shear stress gradient environments.

机译：在高壁切应力和壁切应力梯度环境中内皮细胞凋亡。

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摘要

Vascular diseases like cerebral aneurysms and atherosclerosis are leading causes of mortality worldwide, and account for over 860,000 deaths annually in the United States. The vessel wall is an integrated organ composed of endothelial, smooth-muscle, and fibroblast cells that are active with their function defined by the complex interactions between them. These interactions are integrated signals sent through intercellular communication that are influenced by the local production of mediators such as NO, eNOS, VGEF. These mediators are capable of modifying the structure as well as the function of the vasculature. In addition, the mechanical stimuli generated by blood flow such as wall shear stress, wall shear stress gradient and systemic pressure are known to be major contributing factors in the functioning and maintenance of the endothelial cell (EC) monolayer. Understanding how these mechanical forces affect vessel health is critical to future vascular disease treatment. To this point, most in vitro research on endothelial cells focuses on low (15-30 dyn/cm 2) to normal shear stress environments rather than on the high shear stress and complex impinging flow environments seen at the apices of bifurcations, where intracranial aneurysms usually form.;This study aims at elucidating the EC programmed cell death (apoptosis) response to elevated wall shear stress (WSS), high rate of wall shear stress gradient (WSSG) and the combined effect of WSS and WSSG. For this purpose, a confluent EC monolayer was subjected to flow under a wide range of WSS values, from 15 to 100 dyn/cm2 with negligible gradient, using a tapered chamber and under a T-shaped impingement chamber that mimics the in vivo arterial bifurcations with varying WSS and WSSG values. The flow experiments were run as steady-state, laminar flow for 24 hrs at a constant pressure of 100 mmHg. Apoptosis was examined using TUNEL labeling assay.;In the tapered chamber, the percentage of apoptosis was higher at the regions with physiological WSS magnitudes of 15-30 dyn/cm2 than at regions with high WSS values (>50 dyn/cm2). And, in the impingement chamber the statistical analysis of the data shows that there is a significant effect of WSSG and the combined effect of WSS and WSSG in increasing the percentage of apoptotic cells. These results demonstrate that high WSS (>50 dyn/cm2) does not damage the EC’s but rather suppresses the apoptotic levels but, acts otherwise when combined together with the WSSG. Although further studies are needed, these results provide insight that will allow better understanding of the molecular mechanisms involved in the regulation of the vascular tone and vascular remodeling at high WSS and WSSG environments.
机译：脑动脉瘤和动脉粥样硬化等血管疾病是全球死亡的主要原因，在美国每年导致860,000多例死亡。血管壁是由内皮，平滑肌和成纤维细胞组成的整合器官，它们的功能由它们之间复杂的相互作用所决定。这些相互作用是通过细胞间通信发送的整合信号，受诸如NO，eNOS，VGEF等介体的局部产生影响。这些介体能够改变脉管系统的结构和功能。另外，已知由血流产生的机械刺激，例如壁剪切应力，壁剪切应力梯度和体压是内皮细胞（EC）单层的功能和维持的主要贡献因素。了解这些机械力如何影响血管健康对于将来的血管疾病治疗至关重要。到目前为止，对内皮细胞的大多数体外研究都集中在低（15-30 dyn / cm 2）到正常剪切应力的环境上，而不是在分叉处出现的高剪切应力和复杂的冲击血流环境中，颅内动脉瘤该研究旨在阐明EC程序性细胞死亡（细胞凋亡）对壁剪切应力（WSS）升高，壁剪切应力梯度（WSSG）的高发生率以及WSS和WSSG的联合作用。为此，使用锥形腔室和模仿体内动脉分叉的T形冲击腔室，使融合的EC单层在15到100 dyn / cm2的宽WSS值范围内以可忽略不计的梯度流动。具有变化的WSS和WSSG值。流量实验在100 mmHg的恒定压力下以稳态的层流运行24小时。使用TUNEL标记测定法检查凋亡。在锥形腔中，生理WSS幅度为15-30 dyn / cm2的区域的细胞凋亡百分比高于具有高WSS值（> 50 dyn / cm2）的区域的细胞凋亡百分比。并且，在撞击室中，对数据的统计分析表明，WSSG以及WSS和WSSG的组合作用在增加凋亡细胞百分比方面具有显着作用。这些结果表明，高WSS（> 50 dyn / cm2）不会损害EC，但会抑制细胞凋亡水平，但与WSSG结合使用时，会起到其他作用。尽管需要进一步的研究，但这些结果提供了深刻的见解，将有助于更好地了解在高WSS和WSSG环境下调节血管张力和血管重塑的分子机制。

著录项

  • 作者

    Kaluvala, Shashikanth R.;

  • 作者单位

    State University of New York at Buffalo.;

  • 授予单位 State University of New York at Buffalo.;
  • 学科 Biology Neuroscience.;Engineering Mechanical.
  • 学位 M.S.
  • 年度 2010
  • 页码 61 p.
  • 总页数 61
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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