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.

这个子项目是利用这些资源的众多研究子项目之一