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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Cathepsins F and S block HDL3-induced cholesterol efflux from macrophage foam cells.

In atherosclerosis, accumulation of cholesterol in macrophages may partially depend on its defective removal by high-density lipoproteins (HDL). We studied the proteolytic effect of cathepsins F, S, and K on HDL(3) and on lipid-free apoA-I, and its consequence on their function as inductors of cholesterol efflux from cholesterol-filled mouse peritoneal macrophages in vitro. Incubation of HDL(3) with cathepsin F or S, but not with cathepsin K, led to rapid loss of prebeta-HDL, and reduced cholesterol efflux by 50% in only 1min. Cathepsins F or K partially degraded lipid-free apoA-I and reduced its ability to induce cholesterol efflux, whereas cathepsin S totally degraded apoA-I, leading to complete loss of apoA-I cholesterol acceptor function. These results suggest that cathepsin- secreting cells induce rapid depletion of lipid-poor (prebeta-HDL) and lipid-free apoA-I and inhibit cellular cholesterol efflux, so tending to promote the formation and maintenance of foam cells in atherosclerotic lesions.[1]


  1. Cathepsins F and S block HDL3-induced cholesterol efflux from macrophage foam cells. Lindstedt, L., Lee, M., Oörni, K., Brömme, D., Kovanen, P.T. Biochem. Biophys. Res. Commun. (2003) [Pubmed]
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