Serum cholesterol loading capacity of macrophages is regulated by seropositivity and C-reactive protein in rheumatoid arthritis patients

Excessive cholesterol accumulation in macrophages is the pivotal step underlying atherosclerotic plaque formation. We here explore factors in the serum of patients with RA, and mechanisms through which they interact with and influence cholesterol loading capacity (CLC) of macrophages. In a cross-sec...

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Published in:Rheumatology (Oxford, England) England), 2023-03, Vol.62 (3), p.1254-1263
Main Authors: Karpouzas, George A, Papotti, Bianca, Ormseth, Sarah R, Palumbo, Marcella, Hernandez, Elizabeth, Marchi, Cinzia, Zimetti, Francesca, Budoff, Matthew J, Ronda, Nicoletta
Format: Article
Language:English
Subjects:
Arthritis, Rheumatoid
Atherosclerosis - metabolism
C-Reactive Protein - metabolism
Cholesterol - metabolism
Cross-Sectional Studies
Humans
Immunoglobulin G - metabolism
Lipoproteins, LDL - metabolism
Macrophages - metabolism
Proprotein Convertase 9
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Summary:Excessive cholesterol accumulation in macrophages is the pivotal step underlying atherosclerotic plaque formation. We here explore factors in the serum of patients with RA, and mechanisms through which they interact with and influence cholesterol loading capacity (CLC) of macrophages. In a cross-sectional observational cohort of 104 patients with RA, CLC was measured as intracellular cholesterol content in human THP-1-derived macrophages after incubation with patient serum. Low-density lipoprotein (LDL) oxidation was measured in terms of oxidized phospholipids on apoB100-containing particles (oxPL-apoB100). Antibodies against oxidized LDL (anti-oxLDL), proprotein convertase subtilisin/Kexin type-9 (PCSK9) and high-sensitivity CRP were also quantified. All analyses adjusted for atherosclerotic cardiovascular disease (ASCVD) risk score, obesity, total LDL, statin use, age at diagnosis, and anti-oxLDL IgM. OxPL-apoB100, anti-oxLDL IgG and PCSK9 were positively associated with CLC (all P 
ISSN:1462-0324
1462-0332
DOI:10.1093/rheumatology/keac394