Fiche du document
1 mars 2022
- doi: 10.1242/jcs.258644
- issn: 0021-9533
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1242/jcs.258644
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/34981808
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1477-9137
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_74F4A1CDF17E0
info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/
Sujets proches
Medications Medicaments Prescription drugs Medicines (Drugs) Pharmaceuticals Medicine (Drugs)Citer ce document
A. Zheng et al., « HDLs extract lipophilic drugs from cells. », Serveur académique Lausannois, ID : 10.1242/jcs.258644
Métriques
Partage / Export
Résumé
High-density lipoproteins (HDLs) prevent cell death induced by a variety of cytotoxic drugs. The underlying mechanisms are however still poorly understood. Here, we present evidence that HDLs efficiently protect cells against thapsigargin (TG), a sarco/endoplasmic reticulum (ER) Ca2+-ATPase (SERCA) inhibitor, by extracting the drug from cells. Drug efflux could also be triggered to some extent by low-density lipoproteins and serum. HDLs did not reverse the non-lethal mild ER stress response induced by low TG concentrations or by SERCA knockdown, but HDLs inhibited the toxic SERCA-independent effects mediated by high TG concentrations. HDLs could extract other lipophilic compounds, but not hydrophilic substances. This work shows that HDLs utilize their capacity of loading themselves with lipophilic compounds, akin to their ability to extract cellular cholesterol, to reduce the cell content of hydrophobic drugs. This can be beneficial if lipophilic xenobiotics are toxic but may be detrimental to the therapeutic benefit of lipophilic drugs such as glibenclamide.