Ultrastructural characteristics of the vascular wall components of ruptured atherosclerotic abdominal aortic aneurysm

Abstract

The aim of this study was to determine the ultrastructural characteristics of cell populations and extracellular matrix components in the wall of ruptured atherosclerotic abdominal aortic aneurysm (AAA). We analyzed 20 samples of ruptured AAA. For orientation to the light microscopy, we used routine histochemical techniques by standard procedures. For ultrastructural analysis, we applied transmission electron microscopy (TEM). Our results have shown that ruptured AAA is characterized by the remains of an advanced atherosclerotic lesion in the intima followed by a complete absence of endothelial cells, the disruption of basal membrane and disruption of internal elastic lamina. On plaque margins as well as in the inner media we observed smooth muscle cells (SMCs) that posses a euchromatic nucleus, a well-developed granulated endoplasmic reticulum around the nucleus and reduced myofilaments. The remains of the ruptured lipid core were acellular in all samples; however, on the lateral sides of ruptured plaque we observed a presence of two types of foam cells (FCs), spindle- and star-shaped. Fusiform FCs possess a well-differentiated basal lamina, caveolae and electron dense bodies, followed by a small number of lipid droplets in the cytoplasm. Star-shaped FCs contain a large number of lipid droplets and do not possess basal lamina. On the inner margins of the plaque, we observed a large number of cells undergoing apoptosis and necrosis, extracellular lipid droplets as well as a large number of lymphocytes. The media was thinned out with disorganized elastic lamellas, while the adventitia exhibited leukocyte infiltration. The presented results suggest that atherosclerotic plaque in ruptured AAA contains vascular SMC synthetic phenotype and two different types of FCs: some were derived from monocyte/macrophage lineage, while others were derived from SMCs of synthetic phenotype. The striking plaque hypocellularity was the result of apoptosis and necrosis of different cell populations.

The role of vascular smooth muscle cells in the development of aortic aneurysms and dissections

“…These proteolytic enzymes can degrade the ECM, which facilitates the detachment of vSMC from the ECM and promotes vSMC migration and apoptosis. vSMC phenotypic switching is reported in AAA, 9 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 TAA 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 and TAAD 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 human and rodent studies. An overview of the most important changes and inducers of vSMC phenotypic switching is indicated in Figure 3 .…”

Modern view on the structure of the vascular extracellular matrix

“…These contacts enable the information transfer between connective tissue matrix and integrins on one side and cytoskeleton and nuclei of endothelial cell on the other (5,6). Hence, the information from "outside" can induce either synthesis or degradation of extracellular matrix proteins, control the degree of integrins expression, transduction of signals that can lead to enhanced growth, motility and proliferation of the endothelial cells, as well as regulation of the inflammation (7)(8)(9). Except in the subendothelial layer, significant amount of connective tissue is located in the adventitia.…”

Function of s100 Protein in Coronary Atherosclerosis

“…These cells, due to their neuroectodermal origin, demonstrate S100 protein expression and consequently high affinity for fatty acid binding (Tanaskovic et al, 2019). Coronary arteries that is endothelial, smooth muscle and connective tissue components of their wall, develop from the proepicardial organ, which means that they also originate from the mesenchyme of the splanchopleural mesoderm (Tanaskovic et al, 2011;Tanaskovic et al, 2013).…”