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Updated: Jul 3, 2026

Enrichment of Mammalian Tissues and Xenopus Oocytes with Cholesterol

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Published on: March 25, 2020

Lysobisphosphatidic acid controls endosomal cholesterol levels.

Julien Chevallier¹, Zeina Chamoun¹, Guowei Jiang²

¹Biochemistry, University of Geneva, 30 Quai E. Ansermet, 1211 Geneva 4, Switzerland.

The Journal of Biological Chemistry

|July 23, 2008

Summary

Lysobisphosphatidic acid (LBPA) regulates cholesterol levels within endosomes. This unconventional phospholipid is crucial for managing cholesterol accumulation, particularly in Niemann-Pick type C disease.

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Published on: January 6, 2016

Area of Science:

Cell Biology
Lipid Metabolism
Endosomal Sorting

Background:

Cells primarily acquire cholesterol via low-density lipoprotein endocytosis.
Mechanisms of intra-endosomal cholesterol transport and Niemann-Pick type C (NPC) disease pathogenesis remain unclear.

Purpose of the Study:

To investigate the role of lysobisphosphatidic acid (LBPA) in regulating endosomal cholesterol.
To understand the connection between LBPA, Alix/AlP1, and cholesterol accumulation in NPC.

Main Methods:

Studied the effects of Alix/AlP1 down-expression on LBPA levels and endosomal morphology.
Assessed cellular cholesterol levels in response to altered LBPA and Alix expression.
Investigated the impact of exogenous LBPA on Alix knockdown and NPC cells.

Main Results:

Alix down-expression reduced LBPA levels and lumenal vesicle content in late endosomes, decreasing cellular cholesterol.
Exogenous LBPA restored lumenal membranes and cholesterol in Alix knockdown cells.
Adding LBPA partially reverted the NPC phenotype, indicating LBPA becomes limiting in NPC cells.

Conclusions:

Lysobisphosphatidic acid (LBPA) controls the cholesterol-binding capacity of endosomes.
LBPA, regulated by Alix, plays a critical role in intra-endosomal cholesterol homeostasis.
LBPA is a potential therapeutic target for cholesterol storage disorders like NPC.