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- Title
Plasma from systemic lupus patients compromises cholesterol homeostasis: a potential mechanism linking autoimmunity to atherosclerotic cardiovascular disease.
- Authors
Reiss, Allison B.; Anwar, Kamran; Merrill, Joan T.; Chan, Edwin S. L.; Awadallah, Nahel W.; Cronstein, Bruce N.; Belmont, H. Michael; Belilos, Elise; Rosenblum, Gary; Belostocki, Kristina; Bonetti, Lois; Hasneen, Kowser; Carsons, Steven E.
- Abstract
Atherosclerotic cardiovascular disease (ASCVD) contributes to morbidity and mortality in systemic lupus erythematosus (SLE). Immunologic derangements may disrupt cholesterol balance in vessel wall monocytes/macrophages and endothelium. We determined whether lupus plasma impacts expression of cholesterol 27-hydroxylase, an anti-atherogenic cholesterol-degrading enzyme that promotes cellular cholesterol efflux, in THP-1 human monocytes and primary human aortic endothelial cells (HAEC). THP-1 monocytes and HAEC were incubated in medium containing SLE patient plasma or apparently healthy control human plasma (CHP). SLE plasma decreased 27-hydroxylase message in THP-1 monocytes by 47 ± 8% ( p < 0.008) and in HAEC by 51 ± 5.5% ( n = 5, p < 0.001). THP-1 macrophages were incubated in 25% lupus plasma or CHP and cholesterol-loaded (50 µg ml−1 acetylated low density lipoprotein). Lupus plasma more than doubled macrophage foam cell transformation (74 ± 3% vs. 35 ± 3% for CHP, n = 3, p < 0.001). Impaired cholesterol homeostasis in SLE provides further evidence of immune involvement in atherogenesis. Strategies to inhibit or reverse arterial cholesterol accumulation may benefit SLE patients.
- Subjects
CHOLESTEROL; ISOPENTENOIDS; CUTANEOUS tuberculosis; MONOCYTES; CARDIOVASCULAR disease related mortality
- Publication
Rheumatology International, 2010, Vol 30, Issue 5, p591
- ISSN
0172-8172
- Publication type
Article
- DOI
10.1007/s00296-009-1020-6