IMAGING VULNERABLE PLAQUE IN ATHEROSCLEROTIC MICE

动脉粥样硬化小鼠中易损斑块的成像

• 批准号: 8362630
• 负责人: TATIANA B KRASIEVA
• 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/8362630
• 关键词: A Mouse; Apolipoprotein E; Arterial Fatty Streak; Arterial Intimas; Arteries; Atherosclerosis; Biotechnology; Blood Vessels; Blood flow; Cells; Cellular Structures; Collagen; Deposition; Elastin Fiber; Elements; Fluorescence; Funding; Generations; Grant; Image; Inflammatory; Lasers; Lesion; Lipids; Mus; National Center for Research Resources; Necrosis; Principal Investigator; Progressive Disease; Research; Research Infrastructure; Resources; Rupture; Signal Transduction; Smooth Muscle Myocytes; Source; Thrombosis; United States National Institutes of Health; Vascular calcification; artery occlusion; cost; macrophage; monocyte; second harmonic; two-photon

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. Atherosclerosis is a progressive disease that is characterized by the accumulation of lipids, monocytes, fibrous constituents, and various other inflammatory cells in the arterial wall. These deposits form vascular lesions known as atheromatous plaques, which contain necrotic cores and are separated from the arterial intima by a fibrous cap made up of collagen and smooth muscle cells. When these plaques become vulnerable to rupture, they release the inflammatory elements of the necrotic core into the artery, causing thrombosis and obstruction of arterial blood flow. This study analyzes the progression of atherosclerosis in ApoE-deficient, LDLR KO mice. Specifically, we hope to observe two-photon excited fluorescence (TPEF) signals from elastin fibers of the arterial wall and second-harmonic generation (SHG) signals from collagen in the fibrous caps of the vulnerable plaque regions. We also hope to see various cellular structures (e.g. macrophages, smooth muscle cells) and inflammatory elements (e.g. lipids) within the vascular wall, and perhaps identify varying degrees of vascular calcification.

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。 动脉粥样硬化是一种进行性疾病，其特征是脂质，单核细胞，纤维组成部分和动脉壁中其他各种炎症细胞的积累。 这些沉积物形成称为动脉瘤斑块的血管病变，其中包含坏死核，并通过由胶原蛋白和平滑肌细胞组成的纤维帽与动脉内膜分离。 当这些斑块变得容易破裂时，它们会释放坏死核的炎症元件，从而导致血栓形成和动脉血流阻塞。 这项研究分析了APOE缺陷型LDLR KO小鼠中动脉粥样硬化的进展。 具体而言，我们希望观察到来自动脉壁弹性纤维的两光激发荧光（TPEF）信号，并在脆弱斑块区域的纤维帽中的胶原蛋白和第二谐波产生（SHG）信号。 我们还希望看到各种细胞结构（例如巨噬细胞，平滑肌细胞）和血管壁中的炎症元素（例如脂质），也许可以识别出不同程度的血管钙化。