VASCULAR ENDOTHELIAL GROWTH FACTOR ACTIVITY DYNAMICS

血管内皮生长因子活性动态

• 批准号: 8169475
• 负责人: BERNARD CHOI
• 金额: $ 0.34万
• 依托单位: UNIVERSITY OF CALIFORNIA-IRVINE
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-04-01 至 2011-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8169475
• 关键词: Address; Angiogenesis Inhibitors; Biochemical; Blood Vessels; Blood flow; Chronic; Computer Retrieval of Information on Scientific Projects Database; Computer Simulation; Funding; Gene Expression; Goals; Grant; Injury; Institution; Low-Level Laser Therapy; Malignant Neoplasms; Maps; Methods; Modeling; Monitor; Optics; Pharmaceutical Preparations; Photochemotherapy; Port-Wine Stain; Process; Protocols documentation; Research; Research Personnel; Resources; Rodent; Role; Schedule; Source; Tissues; United States National Institutes of Health; Vascular Endothelial Growth Factors; base; 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. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. 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.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 我们对光疗法的微血管反应的理解还处于起步阶段。 关于该反应的大部分已知信息都来自组织光学的计算模型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，对光损伤的慢性微血管反应可能与模型预测或短期体内实验的预测有很大不同。 具体来说，我们观察到了强大的微血管修复过程，导致微血管网络对光疗法的弹性比之前预测的更强。 我们和其他研究人员已经证明了使用抗血管生成剂来调节微血管对光治疗的反应并增强目标微脉管系统的持续血管关闭的潜力。 这些初步结果使人们对可能使用这种基于光/药物的组合方案来增强癌症的光动力疗法和鲜红斑痣胎记的激光疗法产生了极大的兴奋。 然而，这种组合方法的功效很大程度上取决于两种疗法的适当安排，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。 有了这些信息，就有可能解决以下尚未解答的基本问题：光治疗后基因表达、局部氧合和微脉管系统结构重塑之间的关系是什么？ 抗血管生成药物如何调节这些因素和整体修复反应？ 该项目的目标是定量绘制光损伤的体内血流动力学、组织氧合和血管内皮生长因子 (VEGF) 活性。