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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).
Contributors All authors have made substantial contribution to the conception and design, or analysis and interpretation of data, have drafted the article, or revised it critically for important intellectual content, and have given final approval of the version to be published. There is no one else who fulfils the criteria for authorship but has not been included as an author.
Funding This work was funded with the Finanziamento Ricerca Locale 2012 by University of Parma.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.
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