Abstract
Macrophages obtained from the peritoneal cavity of rabbits were incubated with phosphate-(32)P in order to investigate the synthesis of phospholipid by these cells. After 6 hr of incubation 0.25% of the phosphate added to the medium had been incorporated into phospholipid by the macrophages, mainly into lecithin and sphingomyelin, but partly also into phosphatidyl ethanolamine and inositol phosphatide. The addition of cholesterol to the macrophage suspensions increased the rate of incorporation by 20% with 1 mg of cholesterol added, and 44% with 2.5 mg added. The increase was similar for all the phospholipid fractions, and was not accompanied by any increase in oxygen uptake by the cells. The addition of carbon particles (as a specific check for phagocytic effects) had only a small effect on the rate of incorporation. The data provide support for the concept that cholesterol stimulates phospholipid synthesis by similar cells in the arterial wall during atherogenesis.
Highlights
The addition of cholesterol to the macrophage suspensions increased the rate of incorporation by 20% with 1 mg of cholesterol added, and 440/,with 2.5 mg added
The phospholipid that accumulates in the experimental atheromatous lesion, does so intracellularly in the foam cell [3]; this suggests that during development of experimental atheroma, the phospholipid synthesis that is occurring in the arterial wall takes place in the foam cell
We have studied the incorporation of 32Plabeled phosphate into macrophages in vitro, in order, firstly, to establish that synthesis of phospholipid by macrophages occurs, secondly, to identify the phospholipid synthesized, and thirdly, to determine the effect of cholesterol uptake on this process
Summary
The addition of cholesterol to the macrophage suspensions increased the rate of incorporation by 20% with 1 mg of cholesterol added, and 440/,with 2.5 mg added. The data provide support for the concept that cholesterol stimulates phospholipid synthesis by similar cells in the arterial wall during atherogenesis. Zilversmit and coworkers [1, 2] have demonstrated that this phospholipid accumulation occurs as a result of synthesis in the arterial wall rather than by deposition from the blood. The phospholipid that accumulates in the experimental atheromatous lesion, does so intracellularly in the foam cell [3]; this suggests that during development of experimental atheroma, the phospholipid synthesis that is occurring in the arterial wall takes place in the foam cell. While it cannot be asserted with certainty that the metabolism of such cells is the same as that of arterial wall macrophages or of foam cells, it is likely to be similar. We have studied the incorporation of 32Plabeled phosphate into macrophages in vitro, in order, firstly, to establish that synthesis of phospholipid by macrophages occurs, secondly, to identify the phospholipid synthesized, and thirdly, to determine the effect of cholesterol uptake on this process
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