Key result
Inflammatory cytokines and ox-LDL upregulate macrophage VEGF expression in a dose-dependent manner.
Why the study?
The role of inflammatory cytokines and oxidized LDL in regulating VEGF expression in macrophages within atherosclerotic lesions was not fully understood.
p-value: p=<0.001
Inflammatory cytokines and oxidized LDL upregulate VEGF expression in macrophages, suggesting a potential mechanism for neovascularization in atherosclerotic plaque development.
May link macrophage VEGF to plaque neovascularization; hypothesis-generating in animals and leaves open human relevance.
Vascular endothelial growth factor (VEGF), also known as vascular permeability factor, is a specific mitogen for vascular endothelial cells and causes neovascularization and capillary hyperpermeability. We previously found large amounts of VEGF peptide in areas with many macrophage-derived foam cells adjacent to the lipid core of human atherosclerotic plaques and in basal regions of plaque consisting predominantly of smooth muscle cells. In the present study, we examined the role of inflammatory cytokines and oxidative modified low density lipoprotein (OX-LDL) in the expression of macrophage VEGF. Interleukin 1 beta and tumor necrosis factor alpha upregulated the expression of VEGF mRNA in a macrophage cell line (RAW264). In addition, OX-LDL also upregulated the expression of VEGF mRNA in these cells in a time-dependent and a dose-dependent dependent manner, and there was an increase in the levels of VEGF protein in the conditioned medium. These results suggest that VEGF expression may be upregulated in atherosclerotic lesions and that VEGF may play a role in the development of atherosclerosis.
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Masafumi Kuzuya (1998) studied Atherosclerosis. Inflammatory cytokines (IL-1β, TNF-α) and oxidized LDL (OX-LDL) vs. Control / native LDL was evaluated on VEGF mRNA expression and VEGF protein production (p=<0.001). Inflammatory cytokines (IL-1β, TNF-α) and oxidized LDL significantly upregulated VEGF mRNA expression and protein production in macrophages in a time- and dose-dependent manner.
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