Inhibition of Cholesterol Crystal Formation by Apolipoproteins in Supersaturated Model Bile

Kibe, A; Holzbach, Rüdiger; LaRusso, Nicholas F.; Mao, Shimin

doi:10.1126/science.6429856

Cited by 194 publications

(60 citation statements)

References 18 publications

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“…Apo Al and apo All are secreted in bile (67). Very recently, it was reported that apo Al and apo All in supersaturated gallbladder bile inhibit the rate of formation of solid cholesterol crystals (68). This evidence suggests that the A apolipoproteins can prevent cholesterol gallstone formation.…”

Section: Discussionmentioning

confidence: 89%

Mechanism of action of gemfibrozil on lipoprotein metabolism.

Saku¹,

Gartside²,

Hynd³

et al. 1985

J. Clin. Invest.

185

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Gemfibrozil is a potent lipid regulating drug whose major effects are to increase plasma high density lipoproteins (HDL) and to decrease plasma triglycerides (TG) These data suggest that gemfibrozil increases plasma HDL levels by stimulating their synthesis. Increased transport (turnover) of HDL induced by gemfibrozil may be significant in increasing tissue cholesterol removal in these patients.

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Section: Discussionmentioning

confidence: 89%

Mechanism of action of gemfibrozil on lipoprotein metabolism.

Saku¹,

Gartside²,

Hynd³

et al. 1985

J. Clin. Invest.

185

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“…However, few other details are known about the adsorption process. A better understanding of the antifreeze adsorption may also provide insights into the mechanisms of other proteins that (i) inhibit the growth of biocrystals, such as bone minerals (8,9), enamel (10), cholesterol crystals (11), and kidney stones (12); and (ii) act as crystal nucleators (13,14), since the processes of nucleation and growth inhibition are closely related (13).…”

mentioning

confidence: 99%

Inhibition of growth of nonbasal planes in ice by fish antifreezes.

Raymond

Wilson

DeVries

1989

Proc. Natl. Acad. Sci. U.S.A.

148

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Peptide and glycopeptide antifreezes from a variety of cold-water fishes cause ice single crystals grown from the melt to assume unusual and strikingly similar habits. The antifreezes inhibit growth on the prism faces but allow limited growth on the basal plane. As new layers are deposited on the basal plane, pyramidal surfaces develop on the outside of the crystal, and large hexagonal pits form within the basal plane. The pits are rotated 30' with respect to the normal orientation of hexagonal ice crystals. Growth inhibition on the prism, pyramidal, and pit faces indicates that these faces contain sites of adsorption of the antifreeze molecules. Several properties of

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“…Biliary apoA-I possesses antinucleating properties, although the mechanisms by which apoA-I inhibits cholesterol crystallization and stone formation are not well defined (16,21). ApoA-I is transported from the AP to the BL side of human and murine GBEC (50), although this was not confirmed in our GBEC system (32).…”

Section: Discussionmentioning

confidence: 59%

Cultured gallbladder epithelial cells synthesize apolipoproteins A-I and E

Liu¹,

Tauscher²,

Seo³

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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Gallbladder epithelial cells (GBEC) are exposed to high and fluctuating concentrations of biliary cholesterol on their apical (AP) surface. GBEC absorb and efflux cholesterol, but the mechanisms of cholesterol uptake, intracellular trafficking, and efflux in these cells are not known. We previously reported that ATP binding cassette (ABC)A1 mediates basolateral (BL) cholesterol efflux in cultured polarized GBEC. In addition, the nuclear hormone receptors liver X receptor (LXR)α and retinoid X receptor (RXR) mediate both AP and BL cholesterol efflux. An interesting finding from our previous study was that apolipoprotein (apo)A-I applied to the AP surfaces of cells elicited BL ABCA1-mediated cholesterol efflux. Because ABCA1-mediated cholesterol efflux requires the presence of a cholesterol acceptor, we hypothesized that GBEC synthesize and secrete endogenous apo into the BL compartment. Here, we demonstrate that cholesterol loading of cells with model bile and AP apoA-I treatment is associated with an increase in the synthesis of apoE mRNA and protein. Furthermore, apoE is secreted into the BL compartment. LXRα/RXR ligands stimulate the synthesis of endogenous apoA-I mRNA and protein, as well as apoE mRNA. BL secretion of apoA-I is elicited by LXRα/RXR ligands. Therefore, GBEC synthesize apoA-I and -E and efflux cholesterol using ABCA1- and non-ABCA1- mediated pathways. These processes may alter gallbladder biliary cholesterol concentrations and thereby influence gallstone formation.

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Inhibition of Cholesterol Crystal Formation by Apolipoproteins in Supersaturated Model Bile

Cited by 194 publications

References 18 publications

Mechanism of action of gemfibrozil on lipoprotein metabolism.

Mechanism of action of gemfibrozil on lipoprotein metabolism.

Inhibition of growth of nonbasal planes in ice by fish antifreezes.

Cultured gallbladder epithelial cells synthesize apolipoproteins A-I and E

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