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Published on: March 8, 2018
Lipoprotein-immune complexes and diabetic vascular complications
C Gisinger1, M F Lopes-Virella
1Department of Internal Medicine III, University of Vienna, Austria.
Diabetes
|October 1, 1992
Summary
Stimulating macrophages with red blood cell-low-density lipoprotein complexes (RBC-LDL-IC) increases LDL uptake by upregulating LDL receptors. This leads to cholesterol accumulation and reduced free cholesterol in macrophages, promoting foam cell formation.
Area of Science:
- Cell Biology
- Immunology
- Biochemistry
Background:
- Previous studies demonstrated that HMM incubation with LDL IC causes cellular cholesterol ester (CE) accumulation and macrophage foam cell transformation.
- Macrophage foam cell formation is a key process in atherosclerosis development.
Purpose of the Study:
- To investigate the effect of red blood cell-low-density lipoprotein-immune complexes (RBC-LDL-IC) on macrophage low-density lipoprotein (LDL) uptake.
- To determine the mechanisms underlying changes in LDL receptor activity and cholesterol metabolism in macrophages stimulated with RBC-LDL-IC.
Main Methods:
- Macrophage stimulation with RBC-LDL-IC.
- Scatchard plot analysis to quantify LDL receptor number.
- Measurement of total cellular unesterified cholesterol (T-UC) and LDL-associated UC.
- Assessment of sterol synthesis rates.
Main Results:
- RBC-LDL-IC stimulation significantly increased LDL uptake in macrophages, indicated by a higher LDL receptor number (1267 vs. 352 ng LDL/mg protein).
- A substantial portion (50%) of T-UC was associated with intracellular intact LDL, and free cholesterol levels were reduced in stimulated cells.
- Sterol synthesis was significantly elevated in RBC-LDL-IC-stimulated macrophages (192.8 +/- 22.9 pmol/mg protein vs. 94.8 +/- 11.8).
Conclusions:
- Macrophage uptake of RBC-LDL-IC enhances LDL receptor activity, leading to increased intracellular accumulation of CE and UC.
- This process decreases the regulatory pool of free cholesterol within macrophages.
- The findings suggest that UC associated with nondegraded intracellular LDL is nonregulatory, contributing to foam cell formation.
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