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Deferoxamine stimulates LDLR expression and LDL uptake in HepG2 cells
Johann Guillemot1, Marie-Claude Asselin1, Delia Susan-Resiga1
1Laboratory of Biochemical Neuroendocrinology, Clinical Research Institute of Montreal (IRCM), University of Montreal, Montreal, Quebec, Canada.
Molecular Nutrition & Food Research
|November 19, 2015
Summary
Iron depletion using deferoxamine (DFO) increases LDL receptor expression and uptake in liver cells. This suggests a mechanism for how reducing iron levels lowers cholesterol.
Area of Science:
- Biochemistry
- Molecular Biology
- Cardiovascular Research
Background:
- Iron overload is linked to atherosclerosis development.
- Iron chelators possess antioxidant properties beneficial for cardiovascular health.
- Hepatic iron accumulation promotes cholesterol synthesis, but the impact of iron depletion on cholesterol metabolism remains unclear.
Purpose of the Study:
- To investigate the effect of iron depletion on hepatic cholesterol metabolism.
- To determine if iron chelators influence the expression of genes involved in cholesterol uptake and metabolism.
Main Methods:
- Utilized human hepatocyte cell lines (HepG2, Huh7) and K562 cells.
- Examined the impact of deferoxamine (DFO) on mRNA and protein levels of key cholesterol-related genes.
- Assessed low-density lipoprotein (LDL) receptor (LDLR) expression, cell surface LDLR, and LDL uptake.
Main Results:
- Deferoxamine (DFO) significantly increased LDL receptor (LDLR) mRNA and protein levels in tested cell lines.
- DFO enhanced cell surface LDLR expression and increased LDL uptake in HepG2 cells.
- No modulation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase or sterol regulatory element-binding proteins was observed, indicating a specific effect on LDLR.
Conclusions:
- Deferoxamine (DFO) upregulates LDLR expression through a posttranscriptional mechanism, likely involving mRNA stabilization.
- The enhanced LDLR activity contributes to increased LDL uptake, suggesting a role in the hypocholesterolemic effects of iron reduction.
