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Intracellular transport and esterification of exchangeable cholesterol in cultured human lung fibroblasts.

Identifieur interne : 001131 ( Ncbi/Curation ); précédent : 001130; suivant : 001132

Intracellular transport and esterification of exchangeable cholesterol in cultured human lung fibroblasts.

Auteurs : J P Slotte ; B. Lundberg ; S. Björkerud

Source :

RBID : pubmed:6712979

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English descriptors

Abstract

We have studied the intracellular fate of exchangeable cholesterol in a model system with lipid vesicles (cholesterol/phospholipid mole ratio 1:1) and cultured human lung fibroblasts. Exchangeable [3H]cholesterol in lipid vesicles was readily incorporated into cellular plasma membranes and transported to intracellular esterification sites. The formation of [3H]cholesteryl esters was not affected by cytoskeleton-disrupting drugs. A reduction of cellular pinocytosis by 75% did not reduce the formation of tracer-labelled esters, suggesting that membrane flow due to the energy-dependent pinocytosis is no major contributor to the intracellular transport of molecular cholesterol between plasma membranes and esterification sites. The formation of [3H]cholesteryl esters was not significantly affected by energy poisons (NaF and KCN) but was inhibited (to 50%) by chloroquine at 50 microM. This may indicate that membrane-derived cholesterol passes through the lysosomal compartment on its way to intracellular esterification sites.

DOI: 10.1016/0005-2760(84)90258-3
PubMed: 6712979

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Le document en format XML

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<term>Colchicine (pharmacology)</term>
<term>Cyanides (pharmacology)</term>
<term>Cytochalasin B (pharmacology)</term>
<term>Fluorides (pharmacology)</term>
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<term>Pinocytose ()</term>
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<div type="abstract" xml:lang="en">We have studied the intracellular fate of exchangeable cholesterol in a model system with lipid vesicles (cholesterol/phospholipid mole ratio 1:1) and cultured human lung fibroblasts. Exchangeable [3H]cholesterol in lipid vesicles was readily incorporated into cellular plasma membranes and transported to intracellular esterification sites. The formation of [3H]cholesteryl esters was not affected by cytoskeleton-disrupting drugs. A reduction of cellular pinocytosis by 75% did not reduce the formation of tracer-labelled esters, suggesting that membrane flow due to the energy-dependent pinocytosis is no major contributor to the intracellular transport of molecular cholesterol between plasma membranes and esterification sites. The formation of [3H]cholesteryl esters was not significantly affected by energy poisons (NaF and KCN) but was inhibited (to 50%) by chloroquine at 50 microM. This may indicate that membrane-derived cholesterol passes through the lysosomal compartment on its way to intracellular esterification sites.</div>
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