Abstract
It is a general belief that low-density lipoprotein (LDL) enters from the lumen into the vessel wall and oxidized (oxLDL) and acts as an important pro-atherogenic role in atherosclerosis and the anti-atherogenic substances such as high-density lipoprotein (HDL) and its component apolipoprotein A1 (ApoA1), also enters from the lumen. However, definite in vivo clinical evidence is lacking. We have demonstrated immunohistochemically that native oxLDL, HDL and ApoA1 co-saved in adipocytes in the majority of human pericoronary adipose tissue (PCAT) samples, and obtained marks that they are conveyed by either CD68(+) macrophages or vasa vasorum to the adjacent coronary. These results recommended the existence of before unrecognized storing and supply site of these proteins and that therapies directing the PCAT could be active in stopping human coronary atherosclerosis.
Highlights
It is a general belief that low-density lipoprotein (LDL) and monocytes enters the vascular wall from the lumen, the previous ends up noticeably oxidized low-density lipoprotein and the last macrophages and accumulate oxLDL, after which oxLDL-containing macrophages develop foam cells, while producing collagen-degrading enzymes such as metalloproteases and collagenases which destroy collagen fibers and hypochlorous acid that destroy endothelial cells, resulting in vulnerable plaques [1,2,3,4,5,6]
OxLDL in human pericoronary adipose tissue (PCAT) (Pericoronary Adipose Tissue): By immunohistochemical techniques, we demonstrated that oxLDL is kept in adipocytes of epicardial PCAT, together cytoplasm and plasma membrane (Figures 1-3) [13]
high-density lipoprotein (HDL) co-depositions with oxLDL in PCAT: We found that HDL and oxLDL co-deposit in human PCAT [14]
Summary
It is a general belief that low-density lipoprotein (LDL) and monocytes enters the vascular wall from the lumen, the previous ends up noticeably oxidized low-density lipoprotein (oxLDL) and the last macrophages and accumulate oxLDL, after which oxLDL-containing macrophages develop foam cells, while producing collagen-degrading enzymes such as metalloproteases and collagenases which destroy collagen fibers and hypochlorous acid that destroy endothelial cells, resulting in vulnerable plaques [1,2,3,4,5,6]. It is generally understood that anti-atherogenic substances like high-density lipoprotein (HDL) [7,8] and its module apolipoprotein A1(ApoA1) [9,10,11,12] arrive the vascular intima from the vessel lumen either straight or thru vasa vasorum. Routes of oxLDL to adjacent coronary intima (plaque): OxLDL deposits showed either a diffuse (Figure 1B-1) or dotted pattern in intima (plaque) (Figure 1A-1) [13].
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