Native and oxidized low density lipoproteins modulate mesangial cell apoptosis
1Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, New York, USA.
Kidney International
|November 1, 1996
Summary
High levels of low-density lipoprotein (LDL) can initially increase mesangial cell proliferation but then induce apoptosis, leading to a hypocellular mesangium in glomerulosclerosis.
Area of Science:
- Nephrology
- Cell Biology
- Cardiovascular Research
Background:
- Hyperlipidemia is linked to mesangial hypercellularity in glomerulosclerosis.
- The role of lipids in mesangial cell apoptosis remains unclear.
Purpose of the Study:
- To investigate if low-density lipoprotein (LDL) can induce mesangial cell apoptosis.
- To explore the mechanisms behind LDL-induced mesangial cell apoptosis.
Main Methods:
- In vitro studies using mouse and human mesangial cells.
- Assessing cell proliferation and apoptosis via cell counts, DNA fragmentation assays, ELISA, and RSG-2 mRNA expression.
- Measuring thiobarbituric acid reactive species (TBARS) to assess LDL oxidation.
- Evaluating the effect of superoxide dismutase (SOD) on apoptosis.
Main Results:
- LDL increased mesangial cell proliferation at lower concentrations and induced apoptosis at higher concentrations.
- Oxidized LDL (OX-LDL) significantly enhanced mesangial cell apoptosis.
- LDL-induced apoptosis was mediated by free radical generation, as evidenced by TBARS and attenuation by SOD.
- Similar effects were observed in human mesangial cells.
Conclusions:
- LDL has a dual effect on mesangial cells, promoting proliferation and then apoptosis.
- Oxidation of LDL and free radical generation are key mechanisms in LDL-induced mesangial cell death.
- These findings suggest LDL contributes to the transition from hypercellular to hypocellular mesangium in glomerulosclerosis.
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