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首页> 外文学位 >Major collateral vessels develop from pre-existing small arteries through Rac2/Nox2 independent mechanisms.
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Major collateral vessels develop from pre-existing small arteries through Rac2/Nox2 independent mechanisms.

机译：主要的附带血管是通过Rac2 / Nox2独立机制从先前存在的小动脉发育而来的。

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摘要

There is no consensus on which vascular segment or what size of vessels is most important in the process of collateral growth, the degree to which these vessels can enlarge, or the mechanisms that mediate collateral vessel expansion and its impairment. Chapter I identifies the major collateral vessels that develop in response to femoral arterial occlusion in the pig, rat, and mouse hindlimbs for comparison to humans. Pre-existent small named arteries enlarged ∼2-3-fold to become the major collateral vessels in each species, these major collaterals displayed characteristics similar to large arteries experiencing flow-mediated outward remodeling, and important differences in vascular wall thickness were observed between rodents and pigs. Chapter II utilized Rac2-/- and Nox2-/- mice to investigate the hypothesis that Nox2-NAD(P)H oxidase is required for major collateral growth subsequent to femoral arterial occlusion. Previous studies suggest bone marrow cell (BMC)-derived reactive oxygen species (ROS) produced by the Nox2 subunit of NAD(P)H oxidase plays an important role in neovascularization and recovery of hindlimb perfusion subsequent to femoral arterial occlusion; but did not investigate collateral growth. The hematopoietic cell restricted protein Rac2 has been shown to bind to and activate Nox2-NAD(P)H oxidase and Rac2-/- and Nox2-/- leukocytes display impaired ROS related functions. The data demonstrated that Rac2 and Nox2 are not essential for major collateral growth, but both are important for the recovery of hindlimb perfusion and preservation of distal tissue morphology. Chapter III investigated BMC and antioxidant therapy in the age-related impairment of collateral growth. Aging, like all cardiovascular disease risk factors is associated with elevated ROS and impaired collateral growth. Studies also suggest BMCs promote collateral growth by secreting paracrine factors but elevated ROS may affect the efficacy of BMCs. The data revealed that neither BMC injection nor antioxidant therapy via apocynin enhanced the process of major collateral artery growth in aged mice.
机译：在侧支生长过程中哪个血管段或血管的大小最重要，这些血管的扩张程度或介导侧支血管扩张及其损害的机制尚无共识。第一章确定了在猪，大鼠和小鼠后肢中响应股动脉闭塞而发育的主要侧支血管，以便与人类进行比较。先前存在的小冠状动脉扩大了约2-3倍，成为每个物种的主要侧支血管，这些主要侧支显示出与大动脉相似的特征，经历了流量介导的向外重塑，并且在啮齿动物之间观察到了重要的血管壁厚度差异和猪。第二章利用Rac2-/-和Nox2-/-小鼠研究了股动脉闭塞后主要侧支生长需要Nox2-NAD（P）H氧化酶的假设。先前的研究表明，NAD（P）H氧化酶Nox2亚基产生的骨髓细胞（BMC）衍生的活性氧（ROS）在股动脉闭塞后新生血管的形成和后肢灌注的恢复中起着重要作用。但没有调查抵押品的增长。造血细胞限制蛋白Rac2已显示出结合并激活Nox2-NAD（P）H氧化酶，Rac2-/-和Nox2-/-白细胞显示出与ROS相关的功能受损。数据表明，Rac2和Nox2对主要侧枝生长不是必需的，但对恢复后肢灌注和保留远端组织形态都非常重要。第三章研究了BMC和抗氧化剂治疗与年龄相关的侧支生长损害的方法。像所有心血管疾病危险因素一样，衰老与ROS升高和侧支生长受损有关。研究还表明，BMC通过分泌旁分泌因子促进侧支生长，但ROS升高可能会影响BMC的功效。数据表明，BMC注射或通过载脂蛋白的抗氧化疗法均未增强衰老小鼠主要侧支动脉的生长过程。

著录项

  • 作者

    DiStasi, Matthew Robert.;

  • 作者单位

    Indiana University.;

  • 授予单位 Indiana University.;
  • 学科 Health Sciences Medicine and Surgery.;Biology Physiology.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 155 p.
  • 总页数 155
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 R501;R601;
  • 关键词

  • 入库时间 2022-08-17 11:38:30

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