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Cholesterol transport between cells and high-density lipoproteins
W J Johnson1, F H Mahlberg, G H Rothblat
1Department of Physiology and Biochemistry, Medical College of Pennsylvania, Philadelphia 19129.
Biochimica Et Biophysica Acta
|October 1, 1991
Summary
High-density lipoprotein (HDL) removes cholesterol from cells, a process crucial for preventing atherosclerosis. Specific HDL subfractions efficiently promote cholesterol removal, highlighting their anti-atherogenic potential.
Area of Science:
- Biochemistry and Molecular Biology
- Cardiovascular Research
- Cell Biology
Background:
- High-density lipoprotein (HDL) is recognized for its anti-atherogenic properties, primarily through its role in reverse cholesterol transport.
- Reverse cholesterol transport is the process of removing excess cholesterol from peripheral cells and transporting it to the liver for excretion.
- HDL plays a critical role in mediating sterol transport between cells and the plasma compartment.
Purpose of the Study:
- To review the mechanisms governing sterol movement between HDL and cells.
- To elucidate the processes involved in cholesterol efflux from cells to HDL and intracellular sterol mobilization.
Main Methods:
- Review of existing human and animal studies, cell culture experiments, and biochemical analyses.
- Analysis of sterol transfer dynamics, including diffusion and mediated transport.
- Investigation of HDL subfractions and their role in cholesterol efflux.
Main Results:
- Cholesterol movement between HDL and cells occurs via rapid bidirectional diffusion, primarily at the plasma membrane.
- Net cholesterol efflux from cells is facilitated by plasma membrane sterol enrichment or HDL sterol depletion.
- Specific HDL subfractions (pre-beta mobility, apoA-I containing) show enhanced capacity for promoting cell sterol efflux.
Conclusions:
- Understanding sterol transport mechanisms is key to harnessing HDL's anti-atherogenic potential.
- Mobilization of intracellular cholesterol to the plasma membrane is a critical step, potentially regulated by HDL binding.
- Further research is needed to clarify the balance between cholesterol efflux and influx for specific HDL subfractions.