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Hypercortisolism, endogenous and related to chronic therapies, is associated with increased cardiovascular risk,1 generally attributed to corticosteroid-induced salt retention and hypertension, glucose intolerance, increased appetite and obesity, and hypercholesterolaemia.
We propose a novel mechanism for corticosteroids pro-atherogenic action, namely a direct promotion of foam cell formation.
We investigated the direct effect of hydrocortisone on cholesterol accumulation in a model of human macrophages, based on the THP-1 cells (an acute monocyte leukaemia cell line) that can be differentiated to macrophage phenotype by phorbol 12-myristate 13-acetate treatment and is widely used in foam cell formation studies. Total cholesterol cell content was measured, according to an established protocol,2 with or without preincubation with hydrocortisone, using normal human serum as cholesterol donor, function due mainly to its low density lipoprotein (LDL) content. We found that hydrocortisone treatment significantly enhances cell cholesterol accumulation (figure 1A). Similar results were obtained when hydrocortisone was added to the normal human serum (data not shown).
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