A possible role of cholesterol in membrane adhesion

Ohki, Shinpei; Leonards, Kenneth S.

doi:10.1021/bi00318a030

Cited by 12 publications

(4 citation statements)

References 20 publications

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“…More significantly, aggregation was blocked by a concentration of ADX (0.5 mM) that is sufficient to form a 1:1 complex with P-450,* (Figure 9). Although cholesterol has been reported to be essential for calcium phosphate induced aggregation of phospholipid vesicles (Ohki & Leonards, 1984), it has no effect on the rate or extent of aggregation in this study.…”

Section: Resultscontrasting

confidence: 57%

“…been reported in the literature which promote vesicle aggregation, for example, myelin basic protein (Lampe et al, 1983;Surewicz et al, 1986), tubulin (Kumar et al, 1982), lectins and calcium ions (Hoeckstra et al, 1985), lectin (Orr et al, 1979), and calcium ions (Ohki & Leonards, 1984; Bakas & Disalvo, 1988). The possibility of fusion was investigated by using a fluorescent assay which monitors the mixing of aqueous contents of liposomes.…”

Section: Resultsmentioning

confidence: 99%

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Cytochrome P-450scc induces vesicle aggregation through a secondary interaction at the adrenodoxin binding sites (in competition with protein exchange)

Dhariwal¹,

Kowluru²,

Jefcoate³

1991

Biochemistry

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Addition of bovine adrenal cytochrome P-450scc to small unilamellar dioleoylphosphatidylcholine vesicles (DOPC-SUV) produces a complex sequence of interactions, indicating exceptional cytochrome mobility. First, cholesterol transfer from cytochrome to vesicles indicated rapid dissociation of P-450scc oligomers and integration of monomers into the membrane (delta A 390-420 nm; t1/2 = 2 s). After 10-15 s, P-450scc-induced aggregation of the vesicles starts, as indicated by increased turbidity (delta A 448 or 520 nm; complete in 6-8 min). Fluorescence quenching experiments indicate that this aggregation does not lead to measurable vesicle fusion during this period. Aggregation is prevented by mild heat denaturation of P-450scc, by addition of anti-P-450scc IgG, and also by 1:1 complex formation with the electron donor adrenodoxin (ADX). P-450scc, therefore, links two vesicles through two separate domains involved in, respectively, membrane integration (lipophilic) and ADX binding (charged). Although completely bound by DOPC-SUV, as evidenced by Sephadex elution, P-450scc has access within 1 min to cholesterol in secondary SUV. This is indicated by spectral changes (cholesterol complex formation) and by metabolism of secondary vesicle cholesterol. Since cholesterol equilibrates slowly between vesicles (t1/2 = 1-2 h), these changes arise from P-450scc transfer. This transfer was maximally slowed after a 5-min preincubation with primary vesicles, reflecting more extensive integration into the membrane than is necessary for the rapid initial cholesterol transfer to P-450scc. P-450scc transfer probably results from simultaneous interaction of P-450scc with two vesicles that may also initiate aggregation. Weaker integration into primary dimyristoylphosphatidylcholine vesicles facilitates exchange but prevents aggregation. Integration and aggregation are both enhanced by incorporation of 10% phosphatidylinositol into SUV, while exchange is slowed. This mobility of P-450scc is most probably a consequence of the absence of amino-terminal anchoring. P-450scc-induced association of inner mitochondrial membrane segments may contribute to the exceptionally vesiculated structure of adrenal and ovarian mitochondria that parallels increased P-450scc content.

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Section: Resultscontrasting

confidence: 57%

Section: Resultsmentioning

confidence: 99%

Cytochrome P-450scc induces vesicle aggregation through a secondary interaction at the adrenodoxin binding sites (in competition with protein exchange)

Dhariwal¹,

Kowluru²,

Jefcoate³

1991

Biochemistry

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“…On the other hand, the inner membrane was unable to incorporate cholesterol, demonstrating that the inner membrane has a restricted access to the cytoplasmic cholesterol pool. With respect to this point, it is known that cholesterol plays an important role in some membrane processes, such as membrane adhesion (Ohki and Leonards, 1984) and mitochondrial import of proteins (Hartl et al, 1989). Our results show that, associated with the accumulation of cholesterol in mitochondria, there is an increase in vesicles in the intermembrane space, as reported by Ohlendieck et al (1986).…”

Section: Discussionmentioning

confidence: 99%

Cholesterol increase in mitochondria: its effect on inner-membrane functions, submitochondrial localization and ultrastructural morphology

Echegoyen¹,

Oliva²,

Sepúlveda³

et al. 1993

Biochemical Journal

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The effect of cholesterol incorporation on some functions of the mitochondrial inner membrane and on the morphology of rat liver mitochondria was studied. Basal ATPase and succinate dehydrogenase activities remained unchanged after cholesterol was incorporated into the mitochondria; however, uncoupled ATPase activity was partially inhibited. The presence of several substrates and inhibitors did not change the amount of cholesterol incorporated, which was localized mostly in the outer membrane. Electron-microscope observations revealed the presence of vesicles between the outer and inner membranes; these vesicles increased in number with the amount of cholesterol incorporated. The data suggest that cholesterol induces the formation of vesicles from the outer membrane, and modifies the activity of stimulated ATPase.

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“…Structural parameters change slowly with increasing cholesterol content up to about 32 mol %, and a relatively abrupt structural alteration as revealed by hydrodynamic parameters occurs above this cholesterol content (Newman & Huang, 1975). Cholesterol interacts with phospholipids to decrease the area occupied per phospholipid molecule (Lecuyer & Dervichian, 1969); it also controls the fluidity of bilayers (Demel & DeKruyff, 1976); it induces membrane aggregation by nascent calcium phosphate (Ohki & Leonards, 1984), and it activates the low-pH-triggered membrane fusion activity of Semliki forest virus (Kielian & Helenius, 1984). In our study, we investigate both Ca-induced vesicle aggregation and phosphatidic acid mediated bilayer traversal by calcium ion and find that cholesterol has a large influence on aggregation [trani-Ca(PA)2 formation] but little on calcium traversal [cw-Ca(PA)2 formation].…”

mentioning

confidence: 99%

Effect of cholesterol on calcium-induced aggregation of liposomes and calcium diphosphatidate membrane traversal

Chauhan¹,

Chauhan²,

Brockerhoff³

1986

Biochemistry

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Sonicated cholesterol-phosphatidylcholine (PC) liposomes containing 4 mol % phosphatidic acid (PA) aggregate in 10 mM Ca2+, slowly at low molar fractions of cholesterol (up to 30%) and 15 times faster at higher concentrations; the inflection point is at ca. 35 mol % bilayer cholesterol. O-[[(Methoxyethoxy)ethoxy]ethyl]cholesterol (OH-blocked cholesterol) does not give this rate enhancement. If PC is replaced by diether PC (CO groups abolished), cholesterol does not accelerate aggregation at concentrations in the bilayer below 50 mol %. No change in Ca2+-induced aggregation rates was observed if the ester CO groups of the bridge-forming PA only were replaced by CH2 (diether PA) in liposomes containing PC and cholesterol. PA-mediated Ca2+ membrane traversal seems to be accelerated by the addition of cholesterol to the PC-PA membrane, but analysis shows that the effect is due to the bilayer condensation effect of cholesterol resulting in an increase in the surface concentration of PA and that membrane cholesterol in fact slightly reduces the rate of Ca(PA)2 traversal; OH-blocked cholesterol, however, increases this rate 3-fold. It appears that lipid OH and CO groups interact, directly or with the mediation of water, in establishing the structure of the membrane "hydrogen belts", i.e., the strata containing those hydrogen-bond donors and acceptors. Cholesterol hydroxyl above 33 mol % (saturation of a 2:1 PC/cholesterol complex?) causes a restructuring of the hydrogen belts that facilitates membrane-water-membrane dehydration, the prerequisite for liposome aggregation by trans-Ca(PA)2 formation. On the other hand, the formation of the dehydrated cis-Ca(PA)2 complex that precedes Ca2+ membrane traversal is not accelerated by presence of the cholesterol hydroxyl group.

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A possible role of cholesterol in membrane adhesion

Cited by 12 publications

References 20 publications

Cytochrome P-450scc induces vesicle aggregation through a secondary interaction at the adrenodoxin binding sites (in competition with protein exchange)

Cytochrome P-450scc induces vesicle aggregation through a secondary interaction at the adrenodoxin binding sites (in competition with protein exchange)

Cholesterol increase in mitochondria: its effect on inner-membrane functions, submitochondrial localization and ultrastructural morphology

Effect of cholesterol on calcium-induced aggregation of liposomes and calcium diphosphatidate membrane traversal

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