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.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的主要研究者可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 动脉粥样硬化是一种进行性疾病，其特征是动脉壁中脂质、单核细胞、纤维成分和各种其他炎症细胞的积累。 这些沉积物形成称为动脉粥样斑块的血管病变，其中含有坏死核心，并通过由胶原和平滑肌细胞组成的纤维帽与动脉内膜分开。 当这些斑块变得容易破裂时，它们会将坏死核心的炎症成分释放到动脉中，导致血栓形成和动脉血流阻塞。 本研究分析了 ApoE 缺陷的 LDLR KO 小鼠的动脉粥样硬化进展情况。 具体来说，我们希望观察来自动脉壁弹性蛋白纤维的双光子激发荧光（TPEF）信号和来自易损斑块区域纤维帽中胶原蛋白的二次谐波产生（SHG）信号。 我们还希望看到血管壁内的各种细胞结构（例如巨噬细胞、平滑肌细胞）和炎症成分（例如脂质），并可能识别不同程度的血管钙化。