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Cellular and Molecular Dynamics of the Stressed Myocardium.

机译：应激心肌的细胞和分子动力学。

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摘要

All organisms will be exposed to various types of stress throughout their lifetimes. These can range from exogenous toxins to extreme temperatures and have the potential to destabilize proper cellular function. Cells have adapted ways to respond to various types of stress and do so in an attempt to maintain or reestablish cellular homeostasis. This is especially true of the heart as it must perform its function continuously and consistently throughout the entire lifespan of an organism. The work reported here investigates the effects of stress on the dynamics of heart muscle function. Three models of stress are investigated: (1) acute inflammatory stress, (2) constitutive mitochondrial stress and (3) hyperglycemic stress. By using fluorescent confocal microscopy, immunohistochemistry and digital image processing, I examined the effects of acute inflammatory stress on Ca2+ signaling in neonatal cardiac myocytes. I also explored the therapeutic potential of stem cells in an inflammation paradigm showing that they can elicit both a protective and reparative effect in an inflammation model. I also examined Ca 2+ dynamics and mitochondrial membrane potential stability in adult cardiac myocytes in a model of mitochondrial stress. In this model, I explored the role of mitofusin 2 in the ability of the mitochondrial membrane to resist depolarization as well as its effects on Ca2+ transients and myocyte contraction. Finally, I investigated the effects of acute hyperglycemia on mitochondrial membrane resistance to depolarization and alteration of oxidative state within the cell. This work demonstrates how the heart muscle responds to various environmental stressors and lays the foundation for further exploration into not only these specific stress models but the cardiac cell stress response. We discovered that multiple pathways are involved in the cellular response to stress in heart, often in conjunction with each other. This linkage of stress related pathways in heart should yield fruitful avenues of research for the future.
机译：所有生物在其整个生命周期中都会遭受各种类型的压力。这些可能从外源性毒素到极端温度不等，并可能破坏适当的细胞功能。细胞已经适应了应对各种类型压力的方法，并试图维持或重建细胞体内稳态。对于心脏来说尤其如此，因为心脏必须在有机体的整个生命周期中连续不断地执行其功能。此处报道的工作调查了应激对心肌功能动态的影响。研究了三种应激模型：（1）急性炎症应激；（2）线粒体本构性应激；（3）高血糖应激。通过使用荧光共聚焦显微镜，免疫组织化学和数字图像处理，我检查了急性炎症应激对新生心肌细胞中Ca2 +信号传导的影响。我还探讨了干细胞在炎症范例中的治疗潜力，表明干细胞可以在炎症模型中引起保护和修复作用。在线粒体应激模型中，我还检查了成年心肌细胞中Ca 2+动力学和线粒体膜电位的稳定性。在此模型中，我探讨了线粒体融合蛋白2在线粒体膜抵抗去极化的能力中的作用以及其对Ca2 +瞬变和心肌细胞收缩的影响。最后，我研究了急性高血糖症对线粒体膜对去极化和细胞内氧化态改变的抗性的影响。这项工作证明了心肌如何对各种环境应激源做出反应，并为进一步探索这些特定的应激模型以及心肌细胞应激反应奠定了基础。我们发现，细胞途径对心脏压力的反应涉及多种途径，通常相互结合。心脏中与压力相关的途径之间的这种联系应该为将来的研究提供富有成果的途径。

著录项

  • 作者

    Riley, Dushon.;

  • 作者单位

    University of Maryland, Baltimore.;

  • 授予单位 University of Maryland, Baltimore.;
  • 学科 Biology Physiology.
  • 学位 Ph.D.
  • 年度 2014
  • 页码 155 p.
  • 总页数 155
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 地球物理学;
  • 关键词

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