4.5 Article

Distinct macrophage phenotype and collagen organization within the intraluminal thrombus of abdominal aortic aneurysm

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JOURNAL OF VASCULAR SURGERY
卷 62, 期 3, 页码 585-593

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DOI: 10.1016/j.jvs.2014.11.086

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  1. NHLBI NIH HHS [R01 HL086418, HL-086418] Funding Source: Medline

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Objective: Little is known about the etiologic factors that lead to the occurrence of intraluminal thrombus (ILT) during abdominal aortic aneurysm (AAA) development. Recent work has suggested that macrophages may play an important role in progression of a number of other vascular diseases, including atherosclerosis; however, whether these cells are present within the ILT of a progressing AAA is unknown. The purpose of this work was to define the presence, phenotype, and spatial distribution of macrophages within the ILT excised from six patients. We hypothesized that the ILT contains a population of activated macrophages with a distinct, nonclassical phenotypic profile. Methods: ILT samples were examined using histologic staining and immunofluorescent labeling for multiple markers of activated macrophages (cluster of differentiation [CD] 45, CD68, human leukocyte antigen-DR, matrix metalloproteinase 9) and the additional markers alpha-smooth muscle actin, CD34, CD105, fetal liver kinase-1, and collagen I and III. Results: Histologic staining revealed a distinct laminar organization of collagen within the shoulder region of the ILT lumen and a spatially heterogeneous cell composition within the ILT. Most of the cellular constituents of the ILT were in the luminal region and predominantly expressed markers of activated macrophages but also concurrently expressed alpha-smooth muscle actin, CD105, and synthesized collagen I and III. Conclusions: This report presents evidence for the presence of a distinct macrophage population within the luminal region of AAA ILT. These cells express a set of markers indicative of a unique population of activated macrophages. The exact contributions of these previously unrecognized cells to ILT formation and AAA pathobiology remains unknown.

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