Nonuniform accumulation of lipids in aortic intimal thickening
MedWire News: The accumulation of lipids in the intima plays a role in initiating the inflammatory response in atherosclerosis, research shows.
Moreover, the accumulation of lipids is not distributed uniformly throughout the intima. The juxtaluminal layer represents the intimal 'space' where immune processes are initiated, report investigators.
"The present study suggests that the processes occurring in the earlier stages of atherosclerosis differ in different sublayers of the tunica intima," write Alexander Orekhov (Russian Academy of Natural Sciences, Moscow, Russia) and colleagues in the journal Atherosclerosis.
Previous studies have shown that in addition to smooth muscle cells, the major cell type of the normal arterial intima, immune-inflammatory cells, also resides in the intima. These cells include lymphocytes, dendritic cells, and macrophages.
A number of autopsy studies have also shown that lipids can be found in the arterial intima in sites that do not show any signs of atherosclerotic lesion formation.
These studies have led some to speculate that lipid accumulation in the intima starts a number of cascading reactions that lead to the development of atherosclerotic lesions.
In this study, Orekhov and colleagues analyzed the correlation between lipid deposition, immune-inflammatory cell content and major histocompatibility complex (MHC) class II molecule HLA-DR expression in diffuse intimal thickening (DIT).
There was a nonuniform distribution of lipids throughout the intima. For example, in the juxtaluminal sublayer, the lipids were found extracellularly and intracellularly.
In the juxtamedial musculoelastic sublayer, the lipids were observed primarily along the elastic fibers.
The deposition of lipids was also shown to be positively correlated with HLA-DR expression.
HLA-DR expression is recognized as a marker of immune activation, reflecting the ability of immune-inflammatory cells to present antigen to T cells.
These data showing a positive correlation between lipid deposition and immune-inflammatory cell content in DIT "supports a view that immune-inflammatory cells are responsible for the activation of lymphocytes from the very early stages of atherosclerosis," say Orekhov and colleagues.
The correlation between lipid deposits and the immune-inflammatory cell layer was stronger in the juxtaluminal sublayer than in the juxtamedial musculoelastic layer.
According to the researchers, these results show that the intima of large human arteries is complex tissue that can be divided into sublayers and may play unequal roles in the development of atherosclerosis.
"The present study reinforces a view that in the early stages of atherosclerosis the contribution of the inner juxtaluminal sublayer in immune processes is more profound than that of the external juxtamedial musculoelastic sublayer," they state.
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