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Autoren: Marczynski, Paul
Meineck, Myriam
Xia, Ning
Li, Huige
Kraus, Daniel
Roth, Wilfried
Möckel, Tamara
Boedecker, Simone
Schwarting, Andreas
Weinmann-Menke, Julia
Titel: Vascular inflammation and dysfunction in lupus-prone mice-IL-6 as mediator of disease initiation
Online-Publikationsdatum: 31-Mai-2021
Erscheinungsdatum: 2021
Sprache des Dokuments: Englisch
Zusammenfassung/Abstract: Background: Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease and patients are under an increased risk for cardiovascular (CV) events and mortality. The increased CV risk for patients with SLE seems to be caused by a premature and accelerated atherosclerosis, attributable to lupus-specific risk factors (i.e., increased systemic inflammation, altered immune status), apart from traditional CV risk factors. To date, there is no established experimental model to explore the pathogenesis of this increased CV risk in SLE patients. Methods: Here we investigated whether MRL-Faslpr mice, which develop an SLE-like phenotype, may serve as a model to study lupus-mediated vascular disease. Therefore, MRL-Faslpr, MRL-++, and previously generated Il6−/− MRL-Faslpr mice were used to evaluate vascular changes and possible mechanisms of vascular dysfunction and damage. Results: Contrary to MRL-++ control mice, lupus-prone MRL-Faslpr mice exhibited a pronounced vascular and perivascular leukocytic infiltration in various organs; expression of pro-inflammatory cytokines in the aorta and kidney was augmented; and intima-media thickness of the aorta was increased. IL-6 deficiency reversed these changes and restored aortic relaxation. Conclusion: Our findings demonstrate that the MRL-Faslpr mouse model is an excellent tool to investigate vascular damage in SLE mice. Moreover, IL-6 promotes vascular inflammation and damage and could potentially be a therapeutic target for the treatment of accelerated arteriosclerosis in SLE.
DDC-Sachgruppe: 570 Biowissenschaften
570 Life sciences
610 Medizin
610 Medical sciences
Veröffentlichende Institution: Johannes Gutenberg-Universität Mainz
Organisationseinheit: FB 04 Medizin
Veröffentlichungsort: Mainz
ROR: https://ror.org/023b0x485
DOI: http://doi.org/10.25358/openscience-5927
Version: Published version
Publikationstyp: Zeitschriftenaufsatz
Weitere Angaben zur Dokumentart: Scientific article
Nutzungsrechte: CC BY
Informationen zu den Nutzungsrechten: https://creativecommons.org/licenses/by/4.0/
Zeitschrift: International journal of molecular sciences
22
5
Seitenzahl oder Artikelnummer: 2291
Verlag: Molecular Diversity Preservation International
Verlagsort: Basel
Erscheinungsdatum: 2021
ISSN: 1422-0067
1661-6596
URL der Originalveröffentlichung: https://doi.org/10.3390/ijms22052291
DOI der Originalveröffentlichung: 10.3390/ijms22052291
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