Inhibition of protein kinase Cbeta prevents
foam cell formation by reducing scavenger receptor A expression in human macrophages.
The macrophages get clogged with cholesterol and become what scientists call
foam cells, which are one of the earliest markers of atherosclerosis."
Disrupted fibrous caps are usually heavily infiltrated by macrophage
foam cells and such rupture-related macrophages are activated, indicating ongoing inflammation at the site of plaque disruption.
CRP activates complement through binding to the Fc[gamma] receptor and enhancing phagocytosis of low-density lipoprotein, leading to the formation of
foam cells (Zwaka et al.
Pure, "Lipoproteins, macrophage function, and atherosclerosis: beyond the
foam cell?," Cell Metabolism, vol.
However, SMCs are also transformed into
foam cells when cultured with modified LDL [22], and expression levels and/or patterns of scavenger receptors in macrophages and SMCs are different between C57Bl/6 and ddY mice [23].
Correlation between Macrophage
Foam Cell Formation and Glycemic Control.
Supplementary Figure 1 (in Supplementary Material available online at http://dx.doi.org/10.1155/2016/7124251) shows that, upon incubation of the studied cells with LDL/LDL-FITC for 3 hours, no
foam cell formation was evident.
Atherosclerosis (AS) is an inflammatory disease characterized by lipid accumulation and
foam cell formation by monocyte-derived macrophages and smooth muscle cells (Tabata et al., 2003; Deng et al., 2005).
Inflammatory changes without
foam cell lesions and typical atheromata have also been observed in C.
Necrotic adipose tissue is characterized by
foam cell after the phagocytosis by a large number of macrophages.
During impact, gas is squeezed out of the open
foam cell and energy is dissipated.