Related Experiment Video
Updated: Aug 24, 2026
LDL Cholesterol Uptake Assay Using Live Cell Imaging Analysis with Cell Health Monitoring
Published on: November 17, 2018
Atorvastatin reduces CD68, FABP4, and HBP expression in oxLDL-treated human macrophages
Gemma Llaverias1, Véronique Noé, Silvia Peñuelas
1Department of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Spain.
Abstract:
With the aim of identifying new target genes that could contribute to limit foam cell formation, we analyzed changes in the pattern of gene expression in human THP-1 macrophages treated with atorvastatin and oxidized-LDL (oxLDL). To this end, we used a human cDNA array containing 588 cardiovascular-related cDNAs. Exposure to oxLDL resulted in differential expression of 26 genes, while coincubation with atorvastatin modified the expression of 29 genes, compared to treatment with oxLDL alone. Changes in the expression of candidate genes, potentially connected to the atherosclerotic process, were confirmed by quantitative RT-PCR and Western blot. We show that atorvastatin prevents the increase in the expression of scavenger receptor CD68 and that of fatty acid binding protein 4 caused by oxLDL. In addition, atorvastatin reduces the expression of HDL-binding protein, apolipoprotein E, and matrix metalloproteinase 9. These findings are relevant to understand the direct antiatherogenic effects of statins on macrophages.
Insights
Atorvastatin limits foam cell formation by altering gene expression in macrophages. It reduces key proteins involved in atherosclerosis, offering direct antiatherogenic effects.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Pharmacology
Background:
- Foam cell formation is a key process in atherosclerosis.
- Statins are widely used to manage cardiovascular disease.
- Understanding statins' direct effects on macrophages is crucial.
Purpose of the Study:
- To identify novel target genes influencing foam cell formation.
- To investigate the impact of atorvastatin on gene expression in macrophages exposed to oxidized-low-density lipoprotein (oxLDL).
Main Methods:
- Human THP-1 macrophages were treated with atorvastatin and oxLDL.
- Gene expression profiling was performed using a human cDNA array (588 cardiovascular-related cDNAs).
- Quantitative RT-PCR and Western blot validated changes in candidate gene expression.
Main Results:
- Oxidized-low-density lipoprotein (oxLDL) altered the expression of 26 genes.
- Atorvastatin modified the expression of 29 genes compared to oxLDL alone.
- Atorvastatin inhibited oxLDL-induced increases in scavenger receptor CD68 and fatty acid binding protein 4.
- Atorvastatin reduced the expression of HDL-binding protein, apolipoprotein E, and matrix metalloproteinase 9.
Conclusions:
- Atorvastatin exhibits direct antiatherogenic effects on macrophages.
- The drug modulates key genes involved in lipid metabolism and matrix remodeling.
- Findings provide insights into the molecular mechanisms of statin action in atherosclerosis.
Related Concept Videos
01:20Lipid-Lowering Drugs: Statins and Miscellaneous Agents
01:38Inflammation