Hydrocortisone directly promotes cholesterol accumulation in macrophages
- Daniela Greco1,
- Elda Favari1,
- Maria Pia Adorni1,
- Francesca Zimetti1,
- Rita Gatti2,
- Franco Bernini1,
- Nicoletta Ronda1
- 1Department of Pharmacy, University of Parma, Parma, Italy
- 2Department of Biomedical, Biotechnology and Translational Sciences, University of Parma, Parma, Italy
- Correspondence to Professor Franco Bernini, Department of Pharmacy, University of Parma, Parco Area delle Scienze 27/A, Parma 43124, Italy;
- Received 23 October 2013
- Revised 9 December 2013
- Accepted 21 December 2013
- Published Online First 15 January 2014
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).