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Related Experiment Videos

Inhibition of cellular cholesterol esterification can decrease low density lipoprotein receptor number in human

B Middleton

    Biochemical and Biophysical Research Communications
    |May 29, 1987
    PubMed
    Summary
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    Cholesterol esterification inhibition affects low density lipoprotein (LDL) receptors. Reversible inhibitors cause LDL receptor downregulation by accumulating intracellular cholesterol, while irreversible inhibitors do not.

    Area of Science:

    • Cell Biology
    • Biochemistry
    • Molecular Biology

    Background:

    • Fibroblasts normally regulate low density lipoprotein (LDL) receptors in response to cholesterol levels.
    • Cholesterol esterification is a continuous process in cells, even when cholesterol-deprived.
    • Acyl-CoA: cholesterol acyl-transferase (ACAT) is a key enzyme in cholesterol esterification.

    Purpose of the Study:

    • To investigate the role of cholesterol esterification in regulating LDL receptor expression.
    • To determine if inhibition of cholesterol esterification affects LDL receptor binding and metabolism.
    • To differentiate the effects of reversible versus irreversible ACAT inhibitors on LDL receptors.

    Main Methods:

    • Utilized cholesterol-deprived fibroblasts to induce LDL receptors.

    Related Experiment Videos

  • Administered structurally unrelated ACAT inhibitors: progesterone, trimethylcyclohexanyl mandelate, and 58035.
  • Measured basal cholesterol esterification rates.
  • Assessed specific binding and metabolism of LDL after inhibitor exposure.
  • Examined the time-dependent effects of inhibitors on LDL receptor function.

    • Main Results:

    • Progesterone, trimethylcyclohexanyl mandelate, and 58035 all inhibited basal cholesterol esterification within 1 hour.
    • Progesterone and trimethylcyclohexanyl mandelate (reversible inhibitors) caused decreased LDL binding and metabolism after 17 hours.
    • This downregulation was time-dependent and linked to reversible inhibition of esterification.
    • The irreversible inhibitor 58035 did not affect LDL receptor number.
    • Reversible ACAT inhibition leads to intracellular cholesterol accumulation, triggering LDL receptor downregulation.

    Conclusions:

    • Downregulation of LDL receptors is initiated by the accumulation of cholesterol in a specific intracellular pool.
    • Reversible inhibition of cholesterol esterification by compounds like progesterone and trimethylcyclohexanyl mandelate causes this accumulation.
    • Irreversible inhibition of esterification by 58035 does not lead to the same intracellular cholesterol accumulation or receptor downregulation.