An experiment studies early atheroma development. Lipid streaks on arterial walls are examined microscopically and biochemically to determine their cellular and chemical constituents and the factors promoting their formation. Early lesions show increased attachment of monocytes to the endothelium. The monocytes migrate subendothelially and become macrophages; these macrophages transform themselves into foam cells. Which of the following substances is most likely to be responsible for the transformation of macrophages?
Oxidized LDL can be taken up by a special "scavenger" pathway in macrophages; it also promotes monocyte chemotaxis and adherence. Macrophages taking up the lipid become foam cells that begin to form the fatty streak. Smoking, diabetes mellitus, and hypertension all promote free radical formation, and free radicals increase the degradation of LDL to its oxidized form. About one-third of LDL is degraded to the oxidized form; a higher LDL level increases the amount of oxidized LDL available for uptake into macrophages. C-reactive protein is a marker for inflammation, which can increase with more active atheroma and thrombus formation and predicts a greater likelihood of acute coronary syndromes. Increased homocysteine levels promote atherogenesis through endothelial dysfunction. Lp(a), an altered form of LDL that contains the apo B-100 portion of LDL linked to apo A, promotes lipid accumulation and smooth muscle cell proliferation. Platelet-derived growth factor promotes smooth muscle cell proliferation. VLDL is formed in the liver and transformed in adipose tissue and muscle to LDL.
C-reactive protein
Homocysteine
Lp(a)
Oxidized LDL
Blood Vessels