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Schwarz, M.* ; Meyer, C.E.* ; Löser, A.* ; Lossow, K.* ; Hackler, J.* ; Ott, C.* ; Jager, S.* ; Mohr, I.* ; Eklund, E.A.* ; Patel, A.A.H.* ; Gul, N.* ; Alvarez, S.* ; Altinonder, I.* ; Wiel, C.* ; Maares, M.* ; Haase, H.* ; Härtlova, A.* ; Grune, T.* ; Schulze, M.B.* ; Schwerdtle, T.* ; Merle, U.* ; Zischka, H. ; Sayin, V.I.* ; Schomburg, L.* ; Kipp, A.P.*

Excessive copper impairs intrahepatocyte trafficking and secretion of selenoprotein P.

Nat. Commun. 14:3479 (2023)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Selenium homeostasis depends on hepatic biosynthesis of selenoprotein P (SELENOP) and SELENOP-mediated transport from the liver to e.g. the brain. In addition, the liver maintains copper homeostasis. Selenium and copper metabolism are inversely regulated, as increasing copper and decreasing selenium levels are observed in blood during aging and inflammation. Here we show that copper treatment increased intracellular selenium and SELENOP in hepatocytes and decreased extracellular SELENOP levels. Hepatic accumulation of copper is a characteristic of Wilson’s disease. Accordingly, SELENOP levels were low in serum of Wilson’s disease patients and Wilson’s rats. Mechanistically, drugs targeting protein transport in the Golgi complex mimicked some of the effects observed, indicating a disrupting effect of excessive copper on intracellular SELENOP transport resulting in its accumulation in the late Golgi. Our data suggest that hepatic copper levels determine SELENOP release from the liver and may affect selenium transport to peripheral organs such as the brain.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Golgi-complex; Selenium; Quantification; Glycosylation; Metabolism; Expression; Transport; Proteins; Kidney; Model
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 14, Heft: 1, Seiten: , Artikelnummer: 3479 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Toxicology and Pharmacology (TOX)
POF Topic(s) 30203 - Molecular Targets and Therapies
Forschungsfeld(er) Enabling and Novel Technologies
PSP-Element(e) G-505200-003
Förderungen Formas
Swedish Research Council
Swedish Society for Medical Research
Carl Zeiss Foundation
German Research Foundation (DFG)
DOI 10.1038/s41467-023-39245-3
WOS ID 001061547600017
Scopus ID 85161938456
PubMed ID 37311819
Erfassungsdatum 2023-10-18
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