Hexadecylphosphocholine alters nonvesicular cholesterol traffic from the plasma membrane to the endoplasmic reticulum and inhibits the synthesis of sphingomyelin in HepG2 cells.

doi:10.1016/j.biocel.2008.11.004

Paper

Hexadecylphosphocholine alters nonvesicular cholesterol traffic from the plasma membrane to the endoplasmic reticulum and inhibits the synthesis of sphingomyelin in HepG2 cells.

Published Jun 1, 2009 · C. Marco, J. Jiménez-López, P. Ríos-Marco

The international journal of biochemistry & cell biology

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27

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2

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Abstract

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In Vitro Study

Study Snapshot

Hexadecylphosphocholine disrupts nonvesicular cholesterol traffic and inhibits sphingomyelin synthesis in HepG2 cells, potentially disrupting membrane raft integrity and functionality.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Hexadecylphosphocholine alters nonvesicular cholesterol traffic from the plasma membrane to the endoplasmic reticulum and inhibits the synthesis of sphingomyelin in HepG2 cells.

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References

Cholesterol homeostasis and the escape tendency (activity) of plasma membrane cholesterol.

Excess cholesterol in plasma membranes has a high escape tendency, which serves as a feedback signal to intracellular homeostatic elements to down-regulate cholesterol accretion.

Hexadecylphosphocholine interferes with the intracellular transport of cholesterol in HepG2 cells

Hexadecylphosphocholine disrupts cholesterol homeostasis in HepG2 cells, leading to increased cholesterol synthesis and altered phosphatidylcholine/cholesterol ratio, potentially contributing to its antiproliferative activity.

Plasma Membrane Rafts Complete Cholesterol Synthesis by Participating in Retrograde Movement of Precursor Sterols*

Plasma membrane lipid rafts complete cholesterol biosynthesis by participating in the retrograde movement of precursor sterols back to the endoplasmic reticulum.

Ezetimibe interferes with cholesterol trafficking from the plasma membrane to the endoplasmic reticulum in CaCo-2 cells Published, JLR Papers in Press, May 1, 2007.

Ezetimibe disrupts cholesterol trafficking from the plasma membrane to the endoplasmic reticulum, reducing cholesterol transport into lymph.

Inward Translocation of the Phospholipid Analogue Miltefosine across Caco-2 Cell Membranes Exhibits Characteristics of a Carrier-mediated Process

Miltefosine's oral absorption mechanism involves a carrier-mediated process, with passive diffusion followed by active translocation in the inner membrane leaflet.

Citations