Differential effects of oxidized LDL on apolipoprotein AI and B synthesis in HepG2 cells
| Autor: | Denis Blache, Jean Davignon, Nadine Loreau, Lise Bernier, Emmanuel Bourdon, Laurent Lagrost |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
medicine.medical_specialty
Time Factors Free Radicals Apolipoprotein B Immunoprecipitation Biochemistry Cell Line chemistry.chemical_compound Leucine Physiology (medical) Lipid biosynthesis Internal medicine medicine Humans Secretion RNA Messenger Triglycerides Glyceraldehyde 3-phosphate dehydrogenase Apolipoproteins B Apolipoprotein A-I biology Cholesterol nutritional and metabolic diseases Atherosclerosis Lipids MOPS Lipoproteins LDL Oxygen Endocrinology chemistry Cell culture biology.protein lipids (amino acids peptides and proteins) Cholesterol Esters |
| Zdroj: | Free Radical Biology and Medicine. 41:786-796 |
| ISSN: | 0891-5849 |
| Popis: | Oxidized low-density lipoproteins (Ox-LDL) are key elements in atherogenesis. Apolipoprotein AI (apoAI) is an active component of the antiatherogenic high-density lipoproteins (HDL). In contrast, plasma apolipoprotein B (apoB), the main component of LDL, is highly correlated with coronary risk. Our results, obtained in HepG2 cells, show that Ox-LDL, unlike native LDL, leads to opposite effects on apoB and apoAI, namely a decrease in apoAI and an increase in apoB secretion as evaluated by [(3)H]leucine incorporation and specific immunoprecipitation. Parallel pulse-chase studies show that Ox-LDL impaired apoB degradation, whereas apoAI degradation was increased and mRNA levels were decreased. We also found that enhanced lipid biosynthesis of both triglycerides and cholesterol esters was involved in the Ox-LDL-induced increase in apoB secretion. Our data suggest that the increase in apoB and decrease in apoAI secretion may in part contribute to the known atherogenicity of Ox-LDL through an elevated LDL/HDL ratio, a strong predictor of coronary risk in patients. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect