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Immunoproteasome subunit ß5i/LMP7-deficiency in atherosclerosis
Hewing, Bernd ;  Ludwig, Antje ;  Ludwig, Antje ;  Poetzsch, Max ;  Hannemann, Carmen ;  Petry, Andreas ;  Lauer, Dilyara ;  Goerlach, Agnes ;  Kaschina, Elena ;  Mueller, Dominik N. ;  Baumann, Gert ;  Stangl, Verena ;  Stangl, Karl ;  Wilck, Nicola

HaupttitelImmunoproteasome subunit ß5i/LMP7-deficiency in atherosclerosis
AutorHewing, Bernd
AutorLudwig, Antje
AutorLudwig, Antje
AutorPoetzsch, Max
AutorHannemann, Carmen
AutorPetry, Andreas
AutorLauer, Dilyara
AutorGoerlach, Agnes
AutorKaschina, Elena
AutorMueller, Dominik N.
AutorBaumann, Gert
AutorStangl, Verena
AutorStangl, Karl
AutorWilck, Nicola
Seitenzahl10 S.
Freie SchlagwörterAtherosclerosis; Peripheral vascular disease
DDC610 Medizin und Gesundheit
Auch erschienen inScientific Reports. - 7 (2017), Artikel Nr. 13342
ZusammenfassungManagement of protein homeostasis by the ubiquitin-proteasome system is critical for atherosclerosis development. Recent studies showed controversial results on the role of immunoproteasome (IP) subunit β5i/LMP7 in maintenance of protein homeostasis under cytokine induced oxidative stress. The present study aimed to investigate the effect of β5i/LMP7-deficiency on the initiation and progression of atherosclerosis as a chronic inflammatory, immune cell driven disease. LDLR−/−LMP7−/− and LDLR−/− mice were fed a Western-type diet for either 6 or 24 weeks to induce early and advanced stage atherosclerosis, respectively. Lesion burden was similar between genotypes in both stages. Macrophage content and abundance of polyubiquitin conjugates in aortic root plaques were unaltered by β5i/LMP7-deficiency. In vitro experiments using bone marrow-derived macrophages (BMDM) showed that β5i/LMP7-deficiency did not influence macrophage polarization or accumulation of polyubiquitinated proteins and cell survival upon hydrogen peroxide and interferon-γ treatment. Analyses of proteasome core particle composition by Western blot revealed incorporation of standard proteasome subunits in β5i/LMP7-deficient BMDM and spleen. Chymotrypsin-, trypsin- and caspase-like activities assessed by using short fluorogenic peptides in BMDM whole cell lysates were similar in both genotypes. Taken together, deficiency of IP subunit β5i/LMP7 does not disturb protein homeostasis and does not aggravate atherogenesis in LDLR−/− mice.
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Fachbereich/EinrichtungMedizinische Fakultät Charité - Universitätsmedizin Berlin
Erscheinungsjahr2017
Dokumententyp/-SammlungenWissenschaftlicher Artikel
SpracheEnglisch
RechteCreative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Anmerkungen des AutorsDer Artikel wurde in einer reinen Open-Access-Zeitschrift publiziert.
Erstellt am13.11.2017 - 10:36:14
Letzte Änderung13.11.2017 - 10:38:00
 
Statische URLhttp://edocs.fu-berlin.de/docs/receive/FUDOCS_document_000000028471
DOI10.1038/s41598-017-13592-w
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