Vessels Intima Lesions

The normal arterial wall consists of the intima, media, and adventitia, as illustrated in Fig. 4—3A. The endothelium is located in the intima and consists of a layer of endothelial cells that line the lumen of the artery and form a selective barrier between the vessel wall and blood contents. The internal elastic lamina separates the intima and media, where vascular smooth muscle cells are found. The vascular adventitia comprises the artery s outer layer. Atherosclerotic lesions form in the subendothelial space between the endothelial cells and internal elastic lamina. 

There, also, is interest in dietary monounsaturated fatty acids because of their possible protective effect against oxidation of LDL cholesterol (101). There is appreciable evidence that the uptake of LDL cholesterol and the formation of fatty streaks in the intima of large blood vessels, which is considered an early lesion of atherosclerosis, is enhanced by the oxidation of the LDL cholesterol (102, 103). LDL cholesterol was found to be appreciably more stable to oxidation when subjects were fed diets rich in oleic acid than when fed linoleic acid enriched diets (104-106). 

The term atherosclerosis refers to the focal thickening of the intima of arteries. " The thickened intima consists of muscle cells, connective tissue such as collagen and elastin, mucopolysaccharides, and both intracellular and extracellular lipids. As it progresses to the more advanced condition, degenerating cells and cholesterol crystals are found in the lesions. Plasma proteins, lipoproteins, and the formed elements of blood (platelets, leukocytes, and erythrocytes) are also involved in the development of lesions. Progressive atherosclerosis leads to poor blood flow through blood vessels due to occlusive complications, which also promote the accumulation of formed elements. 

Other immune cells that have been implicated in atherogenesis are natural killer (NK) T-cells (NKTs) and dendritic cells (DCs). NKTs have a key role in innate immunity and have been detected in human and murine atherosclerotic lesions. LDL receptor (LDLR)-deficient mice depleted of functional NKTs exhibit a reduction in lesion formation, indicating that recruitment of these cells into the vessel wall contributes to the development of atherosclerosis (Whitman et al, 2004). DCs have a crucial role in the initiation of immune responses and are key antigen-presenting cells. Although their role in atherosclerosis is still unclear, they have been identified in the intima of human lesions and at arterial branch points in animal models, where they localize with T-cells and macrophages (Lord and Bobryshev, 2002). 

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