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2015 ; 62
(3
): 585-93
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Distinct macrophage phenotype and collagen organization within the intraluminal
thrombus of abdominal aortic aneurysm
#MMPMID26206580
Rao J
; Brown BN
; Weinbaum JS
; Ofstun EL
; Makaroun MS
; Humphrey JD
; Vorp DA
J Vasc Surg
2015[Sep]; 62
(3
): 585-93
PMID26206580
show ga
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 ?-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 ?-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.