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Foam Cells in Atherosclerosis Suppress Inflammation

Last Updated: October 03, 2012.

 

Accumulation of desmosterol underlies homeostatic responses seen in macrophage foam cells

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The formation of macrophage foam cells, which are characteristic of atherosclerotic lesions, correlates with suppression of inflammatory genes, according to a study published in the Sept. 28 issue of Cell.

WEDNESDAY, Oct. 3 (HealthDay News) -- The formation of macrophage foam cells, which are characteristic of atherosclerotic lesions, correlates with suppression of inflammatory genes, according to a study published in the Sept. 28 issue of Cell.

Nathanael J. Spann, Ph.D., from the University of California San Diego in La Jolla, and colleagues examined gene and lipid profiles associated with macrophage foam cell formation in wild-type or genetically engineered mice fed either a normal-cholesterol/normal-fat diet or a high-cholesterol/high-fat "Western"-style diet. The genetically engineered mice fed a high-cholesterol/high-fat diet produced large numbers of macrophage foam cells, which accumulated excess cholesterol as foamy lipid droplets.

The researchers found that the formation of foam cells was associated with changes in hundreds of lipid species and the suppression of inflammatory gene expression. The foam cells contained high levels of desmosterol, the final intermediate in cholesterol production. Regulated accumulation of desmosterol was behind many of the homeostatic responses seen in macrophage foam cells, including activation of LXR target genes, inhibition of SREBP target genes, altered fatty acid metabolism, and suppression of genes involved in inflammatory response.

"These observations suggest that macrophage activation in atherosclerotic lesions results from extrinsic, pro-inflammatory signals generated within the artery wall that suppress homeostatic and anti-inflammatory functions of desmosterol," Spann and colleagues conclude.

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