Lipid composition of the golgi apparatus of rat kidney and liver in comparison with other subcellular organelles

Zambrano, Fernando; Fleischer, Sidney; Fleischer, Becca

doi:10.1016/0005-2760(75)90104-6

Cited by 195 publications

(85 citation statements)

References 30 publications

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“…The complexes are sometimes recognized in the trans-side of the Golgi apparatus, as reported in the pancreatic acinar cell by Orci et al (25). These facts coincide well with the biochemical data that the cholesterol contents in the liver and kidney are the lowest in mitochondria, and somewhat higher in rough microsomes and Golgi apparatus, and the highest in plasma membrane (33). Meldolesi et al (14) also showed biochemically that the membrane of the rough endoplasmic reticulum is markedly lower in cholesterol.…”

Section: Discussionsupporting

confidence: 86%

Freeze-fracture images of distribution of filipin- cholesterol complexes in secretory cells of the anterior pituitary and adrenal medulla of mice.

Fujita

Ishimura

Matsuda

et al. 1982

Acta Histochem. Cytochem

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Section: Discussionsupporting

confidence: 86%

Freeze-fracture images of distribution of filipin- cholesterol complexes in secretory cells of the anterior pituitary and adrenal medulla of mice.

Fujita

Ishimura

Matsuda

et al. 1982

Acta Histochem. Cytochem

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“…To measure the esterification of total cholesterol, we preincubated wild-type and NPC1 mutant cells with [ 3 H]cholesterol for 24 h to radiolabel all cholesterol pools. The [ 3 H]cholesterol equilibrates with cellular cholesterol, the vast majority of which is located in the plasma membrane (19,20). We then washed the cells and incubated them with 25-HC for various times, after which we measured the proportion of cellular [ (21).…”

Section: Resultsmentioning

confidence: 99%

Cyclodextrin overcomes deficient lysosome-to-endoplasmic reticulum transport of cholesterol in Niemann-Pick type C cells

Abi-Mosleh

Infante

Radhakrishnan

et al. 2009

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

162

137

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A handoff model has been proposed to explain the egress from lysosomes of cholesterol derived from receptor-mediated endocytosis of LDL. Cholesterol is first bound by soluble Niemann-Pick C2 (NPC2) protein, which hands off the cholesterol to the N-terminal domain of membrane-bound NPC1. Cells lacking NPC1 or NPC2 accumulate LDL-derived cholesterol in lysosomes and fail to deliver LDL cholesterol to the endoplasmic reticulum (ER) for esterification by acyl-CoA acyltransferase (ACAT) and for inhibition of sterol regulatory element-binding protein cleavage. Here, we support this model by showing that the cholesterol transport defect in NPC1 mutant cells is restricted to lysosomal export. Other cholesterol transport pathways appear normal, including the movement of cholesterol from the plasma membrane to the ER after treatment of cells with 25-hydroxycholesterol or sphingomyelinase. The NPC1 or NPC2 block in cholesterol delivery to the ER can be overcome by 2-hydroxypropyl-␤-cyclodextrin, which leads to a marked increase in ACAT-mediated cholesterol esterification. The buildup of cholesteryl esters in the cytosol is expected to be much less toxic than the buildup of free cholesterol in the lysosomes of patients with mutations in NPC1 or NPC2.cholesterol esterification ͉ NPC1 and NPC2 proteins ͉ sphingomyelinase

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“…According to data obtained from model phospholipid͞cholesterol bilayers, molar cholesterol to phospholipid ratios of 0.12 and 1 should lead to increases in bilayer thickness of 2 and 7 Å, respectively, compared with systems with no cholesterol (18)(19)(20). Thus, the predicted decrease in bilayer thickness on cholesterol depletion would have been Ϸ2 Å (instead of Յ1 Å) for ER and Golgi membranes and Ϸ5 Å (instead of Յ1 Å) for basolateral and apical plasma membranes, given cholesterol-tophospholipid molar ratios of 0.08-0.1, 0.16-0.2, and 0.4-0.76, respectively (22,(48)(49)(50)(51). Our data indicate that the assumption that cholesterol affects the thickness of biological membranes is not valid and suggest that the cholesterol content in cell membranes is not modulated for the purpose of controlling bilayer thickness.…”

Section: Discussionmentioning

confidence: 95%

Modulation of the bilayer thickness of exocytic pathway membranes by membrane proteins rather than cholesterol

Mitra

Ubarretxena-Belandia

Taguchi

et al. 2004

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

403

307

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A biological membrane is conceptualized as a system in which membrane proteins are naturally matched to the equilibrium thickness of the lipid bilayer. Cholesterol, in addition to lipid composition, has been suggested to be a major regulator of bilayer thickness in vivo because measurements in vitro have shown that cholesterol can increase the thickness of simple phospholipid͞cholesterol bilayers. Using solution x-ray scattering, we have directly measured the average bilayer thickness of exocytic pathway membranes, which contain increasing amounts of cholesterol. The bilayer thickness of membranes of the endoplasmic reticulum, the Golgi, and the basolateral and apical plasma membranes, purified from rat hepatocytes, were determined to be 37.5 ؎ 0.4 Å, 39.5 ؎ 0.4 Å, 35.6 ؎ 0.6 Å, and 42.5 ؎ 0.3 Å, respectively. After cholesterol depletion using cyclodextrins, Golgi and apical plasma membranes retained their respective bilayer thicknesses whereas the bilayer thickness of the endoplasmic reticulum and the basolateral plasma membrane decreased by 1.0 Å. Because cholesterol was shown to have a marginal effect on the thickness of these membranes, we measured whether membrane proteins could modulate thickness. Protein-depleted membranes demonstrated changes in thickness of up to 5 Å, suggesting that (i) membrane proteins rather than cholesterol modulate the average bilayer thickness of eukaryotic cell membranes, and (ii) proteins and lipids are not naturally hydrophobically matched in some biological membranes. A marked effect of membrane proteins on the thickness of Escherichia coli cytoplasmic membranes, which do not contain cholesterol, was also observed, emphasizing the generality of our findings.

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Lipid composition of the golgi apparatus of rat kidney and liver in comparison with other subcellular organelles

Cited by 195 publications

References 30 publications

Freeze-fracture images of distribution of filipin- cholesterol complexes in secretory cells of the anterior pituitary and adrenal medulla of mice.

Freeze-fracture images of distribution of filipin- cholesterol complexes in secretory cells of the anterior pituitary and adrenal medulla of mice.

Cyclodextrin overcomes deficient lysosome-to-endoplasmic reticulum transport of cholesterol in Niemann-Pick type C cells

Modulation of the bilayer thickness of exocytic pathway membranes by membrane proteins rather than cholesterol

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