VASCULAR ENDOTHELIAL GROWTH FACTOR ACTIVITY DYNAMICS

血管内皮生长因子活性动态

• 批准号: 8362646
• 负责人: BERNARD CHOI
• 金额: $ 0.51万
• 依托单位: UNIVERSITY OF CALIFORNIA-IRVINE
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-04-01 至 2012-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8362646
• 关键词: Address; Angiogenesis Inhibitors; Biochemical; Biotechnology; Blood Vessels; Blood flow; Chronic; Computer Simulation; Funding; Gene Expression; Goals; Grant; Injury; Lasers; Light; Low-Level Laser Therapy; Maps; Methods; Modeling; Monitor; National Center for Research Resources; Optics; Pharmaceutical Preparations; Photochemotherapy; Port-Wine Stain; Principal Investigator; Process; Protocols documentation; Research; Research Infrastructure; Research Personnel; Resources; Rodent; Role; Schedule; Source; Tissues; United States National Institutes of Health; Vascular Endothelial Growth Factors; base; cancer therapy; cost; in vivo; infancy; repaired; research study; response; tissue oxygenation

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Our understanding of the microvascular response to light-based therapy is in its infancy. Much of what is known about the response is derived from computational modeling of tissue optics and short-term (<24 h) monitoring of rodent microvasculature. Recently, we have demonstrated that the chronic microvascular response to light-based injury can differ substantially from that predicted with modeling or from short-term in vivo experiments. Specifically, we have observed a robust microvascular repair process, resulting in a stronger resiliency of the microvascular network to light-based therapy than previously predicted. We and other investigators have demonstrated the potential of using antiangiogenic agents to modulate the microvascular response to light-based therapy and enhance persistent vascular shutdown of the targeted microvasculature. These preliminary results have generated a great deal of excitement for the possible use of this combined light-/drug-based protocol to enhance photodynamic therapy of cancer and laser therapy of port wine stain birthmarks. However, the efficacy of this combined method is strongly dependent on the appropriate scheduling of the two therapies, which currently is unknown. To address this problem, it is necessary to understand the role of biochemical factors in the overall microvascular repair process. With such information, it will become possible to address the following fundamental unanswered questions: What is the relationship between gene expression, local oxygenation, and structural remodeling of the microvasculature after light-based therapy? How do antiangiogenic agents modulate these factors and the overall repair response? The goal of this project is to map quantitatively the in vivo dynamics of blood flow, tissue oxygenation, and vascular endothelial growth factor (VEGF) activity to light-based injury.

该副本是利用资源的众多研究子项目之一 由NIH/NCRR资助的中心赠款提供。对该子弹的主要支持 而且，副投影的主要研究员可能是其他来源提供的 包括其他NIH来源。 列出的总费用可能 代表subproject使用的中心基础架构的估计量， NCRR赠款不直接向子弹或副本人员提供的直接资金。 我们对微血管对光基疗法的反应的理解仍处于起步阶段。 关于响应的许多知识来自组织光学的计算建模和啮齿动物微脉管系统的短期（<24小时）监测。 最近，我们已经证明，慢性微血管对光基损伤的反应可能与建模或短期体内实验预测的损伤可能有很大不同。 具体而言，我们已经观察到了强大的微血管修复过程，从而使微血管网络对基于光的治疗的弹性比以前的预测更强。 我们和其他研究人员已经证明了使用抗血管生成剂调节对光基疗法的微血管反应的潜力，并增强了靶向微脉管系统的持续血管关闭。 这些初步结果引起了极大的兴奋，可以使用这种基于轻/药物的组合方案来增强癌症的光动力疗法和港口葡萄酒染色胎记的激光治疗。 但是，这种组合方法的功效在很大程度上取决于两种疗法的适当调度，这目前尚不清楚。 为了解决这个问题，有必要了解生化因素在整个微血管修复过程中的作用。 有了这样的信息，将有可能解决以下基本未解决的问题：基因表达，局部氧合和基于光基疗法后微脉管系统的结构重塑之间的关系是什么？ 抗血管生成剂如何调节这些因素和总体修复反应？ 该项目的目的是定量地绘制血流，组织氧合和血管内皮生长因子（VEGF）活性的体内动力学，以绘制基于光损伤。