Hydrophobic/hydrophilic balance of proteins: a major determinant of cholesterol crystal formation in model bile.

Ahmed, Hafez; Petroni, Maria Letizia; Abu-Hamdiyyah, Mohammed.; Jazrawi, R. P.; Northfield, T.C.

doi:10.1016/s0022-2275(20)41209-x

Cited by 28 publications

(5 citation statements)

References 33 publications

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“…The secreted vesicles are partially solubilized to form mixed micelles, and this process leads to the formation of highly metastable CH-rich vesicles (Cohen et al, 1990). According to the equilibrium BS−L−H 2 O phase diagram, the transition from lamellar vesicles to micelles transverses two coexistence regions that contain the hexagonal phase, which consists of hexagonally-packed infinitely long cylinders (Small et al, 1966). At the lecithin concentration used in this study (1 mM or ∼0.08 wt %), those transitions occur at approximately 3.5 mM and 3.8 mM TC, respectively (Figure ).…”

Section: Discussionmentioning

confidence: 99%

“…These effects may explain why bile becomes more metastable with increasing total BS/L (Kibe et al, 1985;Harvey et al, 1987). By the same token, amphiphilic proteins can possibly become "secondary" pro-nucleators by either exercising their surfaceactive properties (Ahmed et al, 1994) or acting as transfer carriers that facilitate aqueous diffusion of CH and L monomers (Corradini et al, 1991).…”

Section: R E )mentioning

confidence: 99%

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Structural Mechanisms of Bile Salt-Induced Growth of Small Unilamellar Cholesterol−Lecithin Vesicles

1997

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The liver secretes cholesterol and lecithin in the form of mixed vesicles during the formation of bile. When exposed to bile salts, these metastable vesicles undergo various structural rearrangements. We have examined the effects of three different bile salts, taurocholate (TC), tauroursodeoxycholate (TUDC), and taurodeoxycholate (TDC), on the stability of sonicated lecithin vesicles containing various amounts of cholesterol. Vesicle growth was probed by turbidity measurements, quasi-elastic light scattering, and a resonance energy transfer lipid-mixing assay. Leakage of internal contents was monitored by encapsulation of fluorescence probes in vesicles. At low bile salt-to-lecithin ratios (TC/L or TUDC/L < 1), pure lecithin vesicles do not grow, but exhibit slow intervesicular mixing of lipids as well as gradual leakage. At high BS/L (TC/L or TUDC/L > 5), pure lecithin vesicles are solubilized into mixed micelles with a concomitant decrease in the overall particle size. In this regime, extensive leakage and lipid mixing occur instantaneously after exposure to bile salt. At intermediate BS/L (1 < TC/L or TUDC/L < 5), vesicles grow with time, and the rates of both leakage and lipid mixing are rapid. The data suggest that vesicles grow by the transfer of lecithin and cholesterol via diffusion in the aqueous medium. The addition of cholesterol to lecithin vesicles reduces leakage dramatically and increases the amount of BS required for complete solubilization of vesicles. The more hydrophobic TDC induces vesicle growth at a lower BS/L than does TC or TUDC. These results demonstrate the physiologic forms of lipid microstructures during bile formation and explain how the hydrophilic-hydrophobic balance of BS mixtures may profoundly affect the early stages of CH gallstone formation.

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Section: Discussionmentioning

confidence: 99%

Section: R E )mentioning

confidence: 99%

Structural Mechanisms of Bile Salt-Induced Growth of Small Unilamellar Cholesterol−Lecithin Vesicles

1997

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“…5). On the basis of published work of Ahmed et al (53), we hypothesized (23) that hydrophilic or hydrophobic proteins, as determined by their elution times on a phenyl-agarose column, may produce proor anti-nucleating/crystallizing effects by shifting phase and ACh (᭺) crystal numbers for samples IV. Because samples IV with addition of mucin gel became very sticky and Ch crystallization occurred rapidly (liquid crystal within 6 h and ChM crystal within 14 h), solid Ch crystal number increased appreciably over the following 24 h. CSI values (see Table 1) were significantly higher (P Ͻ 0.05) in samples V (CSI ϭ 2.0) than samples I-IV (CSI ϭ 1.6).…”

Section: Ch Content Mucin Gel and Soluble Biliary Glycoproteins Do Not Influence Ch Crystallization Sequences Or Phase Boundariesmentioning

confidence: 99%

No pathophysiologic relationship of soluble biliary proteins to cholesterol crystallization in human bile

Wang

Cohen²,

Lammert³

et al. 1999

Journal of Lipid Research

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This study explores the pathophysiologic effects of soluble biliary glycoproteins in comparison to mucin gel and cholesterol content on microscopic crystal and liquid crystal detection times as well as crystallization sequences in lithogenic human biles incubated at 37 ؇ C. Gallbladder biles from 13 cholesterol gallstone patients were ultracentrifuged and microfiltered (samples I). Total biliary lipids were extracted from portions of samples I, and reconstituted with 0.15 m NaCl (pH 7.0) (samples II). Portions of samples II were supplemented with purified concanavalin A-binding biliary glycoproteins (final concentration ‫؍‬ 1 mg/mL) (samples III), or mucin gel (samples IV), respectively, isolated from the same cholesterol gallstone biles. Samples V consisted of extracted biliary lipids from uncentrifuged and unfiltered bile samples reconstituted with 0.15 m NaCl (pH 7.0). Analytic lipid compositions of samples I through IV were identical for individual biles but, as anticipated, samples V displayed significantly higher cholesterol saturation indexes. Detection times of cholesterol crystals and liquid crystals were accelerated in the rank order of samples: IV Ͼ V Ͼ I ‫؍‬ II ‫؍‬ III, indicating that total soluble biliary glycoproteins in pathophysiologic concentration had no appreciable effect. Crystallization sequences ( D. Q-H. Wang and M. C. Carey. J. Lipid Res . 1996. 37: 606-630; and 2539-2549) were similar among samples I through V. Crystal detection times and numbers of solid cholesterol crystals were accelerated in proportion to added mucin gel and the cholesterol saturation of bile only. For pathophysiologically relevant conditions, our results clarify that mucin gel and cholesterol content, but not soluble biliary glycoproteins, promote cholesterol crystallization in human gallbladder bile.

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“…between them is of importance for the propensity of gallbladder bile to nucleate cholesterol. It has been proposed that the more hydrophobic protein, the higher the antinucleating potency and vice versa (Ahmed et al, 1994). There are apparently several unidentified proteins in bile and identification of these proteins could be of interest in understanding gallstone formation.…”

Section: Harald Tschesche Bimolecular Interaction Of Matrix Metalloproteinases and Their Inhibitors Timps (Bielefeld University Germany)mentioning

confidence: 99%

MPSA Short Communications Listing

1998

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rh S. Tsiftsoglou TNF-A) Protein Produced Using E. coli Protein Expression System 6. Gerd-J. Krauss, Sieglinde Cavity-Supported HPLC of cis/trans Isomers of Protein-Containing Friebe, and Sabine Gebauer Peptides Using Cyclodextrins an Calixarenes 7. A.G. Lapko and K. Ruckpaul Discrimination of Conformational States of Mitochondrial Cytochrome P-450scc by Selective Modification of Several Lys Residues 8. Stergios A. Lazos and Asterios Production and Purification of Recombinant Human Cytokines (rhIL-4, S. Tsiftsoglou rhGM-CSF, and rhlL-lB) from Genetically Engineered E. coli Cells Bearing pMAL Expression Vector Constructs 9.

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Hydrophobic/hydrophilic balance of proteins: a major determinant of cholesterol crystal formation in model bile.

Cited by 28 publications

References 33 publications

Structural Mechanisms of Bile Salt-Induced Growth of Small Unilamellar Cholesterol−Lecithin Vesicles

Structural Mechanisms of Bile Salt-Induced Growth of Small Unilamellar Cholesterol−Lecithin Vesicles

No pathophysiologic relationship of soluble biliary proteins to cholesterol crystallization in human bile

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