Depletion of L-cell sterol depresses endocytosis

Heiniger, H J; Kandutsch, Andrew A.; Chen, Harry W.

doi:10.1038/263515a0

Cited by 108 publications

(46 citation statements)

References 15 publications

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“…Finally, we determined that the heavy, intermediate, and light subunits of the Gal/ GalNAc adherence lectin partially purify with the detergent- In other systems, it is established that cholesterol-rich membrane domains play a role in endocytosis. Reduction of cholesterol by inhibiting its synthesis with oxygenated cholesterol derivatives was shown to decrease pinocytic rates in L cells (23,24). More recently, the uptake of an apoptotic agent alkyllysophospholipid or the transferrin receptor was blocked by treatment with MBCD or filipin (63).…”

Section: Discussionmentioning

confidence: 99%

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Involvement of Raft-Like Plasma Membrane Domains of Entamoeba histolytica in Pinocytosis and Adhesion

Laughlin¹,

McGugan

Powell

et al. 2004

Infect Immun

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Lipid rafts are highly ordered, cholesterol-rich, and detergent-resistant microdomains found in the plasma membrane of many eukaryotic cells. These domains play important roles in endocytosis, secretion, and adhesion in a variety of cell types. The parasitic protozoan Entamoeba histolytica, the causative agent of amoebic dysentery, was determined to have raft-like plasma membrane domains by use of fluorescent lipid analogs that specifically partition into raft and nonraft regions of the membrane. Disruption of raft-like membrane domains in Entamoeba with the cholesterol-binding agents filipin and methyl-␤-cyclodextrin resulted in the inhibition of several important virulence functions, fluid-phase pinocytosis, and adhesion to host cell monolayers. However, disruption of raft-like domains did not inhibit constitutive secretion of cysteine proteases, another important virulence function of Entamoeba. Flotation of the cold Triton X-100-insoluble portion of membranes on sucrose gradients revealed that the heavy, intermediate, and light subunits of the galactose-N-acetylgalactosamine-inhibitible lectin, an important cell surface adhesion molecule of Entamoeba, were enriched in cholesterol-rich (raft-like) fractions, whereas EhCP5, another cell surface molecule, was not enriched in these fractions. The subunits of the lectin were also observed in high-density, actin-rich fractions of the sucrose gradient. Together, these data suggest that pinocytosis and adhesion are raft-dependent functions in this pathogen. This is the first report describing the existence and physiological relevance of raft-like membrane domains in E. histolytica.Recent evidence suggests that plasma membrane lipids are nonhomogeneously distributed and that microdomains with specialized functions exist in the membrane. One such domain, a lipid raft, is a highly ordered, less-fluid, and tightly packaged membrane domain enriched in cholesterol (or other sterols), glycosphingolipids, and phospholipids with a higher degree of saturated fatty acyl chains than those of the rest of the membrane (reviewed in references 37 and 54). These domains are also detergent insoluble and are thus often referred to as detergent-resistant membranes (DRMs). The presence of microdomains in membranes allows for the inclusion or exclusion of membrane proteins based on their attachment to the membrane via lipid anchors or specific protein-lipid interactions. For example, proteins that are modified with a hydrophobic attachment, such as a glycosylphosphatidylinositol (GPI) anchor, or double acylation or transmembrane proteins with the capacity to interact with cholesterol are often found in lipid microdomains.The physiological role of lipid rafts has been the subject of numerous recent studies, and it has recently become clear that these membrane regions play an important role in a variety of cellular functions, including polarization, signal transduction, endocytosis, secretion, and cell-cell and cell-pathogen adhesion (17,18,21,34,36,44). A range of cell surface receptors m...

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Section: Discussionmentioning

confidence: 99%

“…For example, depletion of cholesterol from the membrane results in the inhibition of pinocytosis (23,24), particularly caveolin-and clathrin-coated pit internalization (59,67). More recently, a requirement for cholesterol has been identified for macropinocytosis in A431 epidermoid carcinoma cells (17).…”

mentioning

confidence: 99%

Involvement of Raft-Like Plasma Membrane Domains of Entamoeba histolytica in Pinocytosis and Adhesion

Laughlin¹,

McGugan

Powell

et al. 2004

Infect Immun

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“…In fact, filipin, which does not affect uptake from clathrin-coated pits, increased the toxicity of diphtheria toxin (Orlandi and Fishman, 1998). Heiniger et al (1976) reported that L cells, in which hydroxymethylglutaryl-CoA reductase activity and cholesterol synthesis were inhibited by addition of 25-hydroxycholesterol, had a reduced rate of endocytosis of the fluid-phase marker HRP. The uptake of HRP was restored by the addition of cholesterol (Heiniger et al, 1976).…”

Section: Role Of Cholesterol In Endocytosismentioning

confidence: 99%

“…Heiniger et al (1976) reported that L cells, in which hydroxymethylglutaryl-CoA reductase activity and cholesterol synthesis were inhibited by addition of 25-hydroxycholesterol, had a reduced rate of endocytosis of the fluid-phase marker HRP. The uptake of HRP was restored by the addition of cholesterol (Heiniger et al, 1976). HRP is endocytosed, however, by both clathrin-dependent and clathrin-independent endocytosis (Oliver, 1982), and the fact that cholesterol depletions of L cells seem to have a stronger effect on total endocytosis in these cells (50%) than the effect we observed on HRP endocytosis in the cell types we have tested could be due to a larger proportion of uptake by clathrin-dependent endocytosis in L cells.…”

Section: Role Of Cholesterol In Endocytosismentioning

confidence: 99%

“…Earlier studies have suggested a role for cholesterol in endocytosis (Heiniger et al, 1976); however, the type of endocytosis affected by cholesterol depletion was not investigated. Cholesterol present in the membrane of mammalian cells is required for normal cellular function (Bloch, 1991) and either is delivered from low-density lipoproteins internalized by recep-tor-mediated endocytosis via clathrin-coated pits followed by subsequent hydrolysis in lysosomes (Brown and Goldstein, 1980) or is synthesized in the endoplasmic reticulum (Reinhart et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

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Extraction of Cholesterol with Methyl-β-Cyclodextrin Perturbs Formation of Clathrin-coated Endocytic Vesicles

Rodal

Skretting

Garred

et al. 1999

MBoC

938

776

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The importance of cholesterol for endocytosis has been investigated in HEp-2 and other cell lines by using methyl-␤-cyclodextrin (M␤CD) to selectively extract cholesterol from the plasma membrane. M␤CD treatment strongly inhibited endocytosis of transferrin and EGF, whereas endocytosis of ricin was less affected. The inhibition of transferrin endocytosis was completely reversible. On removal of M␤CD it was restored by continued incubation of the cells even in serum-free medium. The recovery in serum-free medium was inhibited by addition of lovastatin, which prevents cholesterol synthesis, but endocytosis recovered when a water-soluble form of cholesterol was added together with lovastatin. Electron microscopical studies of M␤CD-treated HEp-2 cells revealed that typical invaginated caveolae were no longer present. Moreover, the invagination of clathrin-coated pits was strongly inhibited, resulting in accumulation of shallow coated pits. Quantitative immunogold labeling showed that transferrin receptors were concentrated in coated pits to the same degree (approximately sevenfold) after M␤CD treatment as in control cells. Our results therefore indicate that although clathrin-independent (and caveolae-independent) endocytosis still operates after removal of cholesterol, cholesterol is essential for the formation of clathrin-coated endocytic vesicles.

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Synthesis of Photoresponsive Fast Self‐healing Polyolefin Composites by Nickel‐Catalyzed Copolymerization of Ethylene and Lignin Cluster Monomers

Chen,

Zou

et al. 2024

Angewandte Chemie

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Polymers may suffer from sudden mechanical damages during long‐term use under various harsh operating environments. Rapid and real‐time self‐healing will extend their service life, which is particularly attractive in the context of circular economy. In this work, a lignin cluster polymerization strategy (LCPS) was designed to prepare a series of lignin functionalized polyolefin composites with excellent mechanical properties through nickel catalyzed copolymerization of ethylene and lignin cluster monomers. These composites can also achieve rapid self‐healing within 30 seconds under a variety of extreme usage environments (underwater, seawater, extremely low temperatures as low as ‐60 °C, organic solvents, acid alkali solvents, etc.), which is of great significance for real‐time self‐healing of sudden mechanical damage. More importantly, the dynamic cross‐linking network within these composites enable great re‐processability and amazing sealing performances.

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Depletion of L-cell sterol depresses endocytosis

Cited by 108 publications

References 15 publications

Involvement of Raft-Like Plasma Membrane Domains of Entamoeba histolytica in Pinocytosis and Adhesion

Involvement of Raft-Like Plasma Membrane Domains of Entamoeba histolytica in Pinocytosis and Adhesion

Extraction of Cholesterol with Methyl-β-Cyclodextrin Perturbs Formation of Clathrin-coated Endocytic Vesicles

Synthesis of Photoresponsive Fast Self‐healing Polyolefin Composites by Nickel‐Catalyzed Copolymerization of Ethylene and Lignin Cluster Monomers

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