A key element of heart disease is the accumulation of immune cells called macrophages that are filled with cholesterol, which gives the cells a foamy appearance. Researchers have identified a network of 46 proteins in macrophages whose regulation is linked to the conversion into 'foam cells', which contribute to atherosclerosis — the thickening of artery walls.
Jay Heinecke and his colleagues at the University of Washington in Seattle used mass spectrometry to identify 777 proteins in macrophages. They then narrowed down the list to the 46 proteins that exhibited a notable increase or decrease in levels when macrophages became foamy. They mapped the proteins into a network by mining protein-interaction databases.
The authors found that regulation of this network was altered in cells treated with drugs that target heart disease, and that apolipoprotein E, a protein known to block atherosclerosis, is a key regulator of the network.