Gutenberg Open Science: Vascular inflammation and dysfunction in lupus-prone mice-IL-6 as mediator of disease initiation

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-5927

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DC Field	Value	Language
dc.contributor.author	Marczynski, Paul	-
dc.contributor.author	Meineck, Myriam	-
dc.contributor.author	Xia, Ning	-
dc.contributor.author	Li, Huige	-
dc.contributor.author	Kraus, Daniel	-
dc.contributor.author	Roth, Wilfried	-
dc.contributor.author	Möckel, Tamara	-
dc.contributor.author	Boedecker, Simone	-
dc.contributor.author	Schwarting, Andreas	-
dc.contributor.author	Weinmann-Menke, Julia	-
dc.date.accessioned	2021-05-31T09:40:42Z	-
dc.date.available	2021-05-31T09:40:42Z	-
dc.date.issued	2021	-
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/5936	-
dc.description.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.	en_GB
dc.description.sponsorship	Open Access-Publizieren Universität Mainz / Universitätsmedizin Mainz	de
dc.language.iso	eng	de
dc.rights	CC BY	*
dc.rights.uri	https://creativecommons.org/licenses/by/4.0/	*
dc.subject.ddc	570 Biowissenschaften	de_DE
dc.subject.ddc	570 Life sciences	en_GB
dc.subject.ddc	610 Medizin	de_DE
dc.subject.ddc	610 Medical sciences	en_GB
dc.title	Vascular inflammation and dysfunction in lupus-prone mice-IL-6 as mediator of disease initiation	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-5927	-
jgu.type.contenttype	Scientific article	de
jgu.type.dinitype	article	en_GB
jgu.type.version	Published version	de
jgu.type.resource	Text	de
jgu.organisation.department	FB 04 Medizin	de
jgu.organisation.number	2700	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.journal.title	International journal of molecular sciences	de
jgu.journal.volume	22	de
jgu.journal.issue	5	de
jgu.pages.alternative	2291	de
jgu.publisher.year	2021	-
jgu.publisher.name	Molecular Diversity Preservation International	de
jgu.publisher.place	Basel	de
jgu.publisher.uri	https://doi.org/10.3390/ijms22052291	de
jgu.publisher.issn	1422-0067	de
jgu.publisher.issn	1661-6596	de
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	570	de
jgu.subject.ddccode	610	de
jgu.publisher.doi	10.3390/ijms22052291
jgu.organisation.ror	https://ror.org/023b0x485
Appears in collections:	JGU-Publikationen

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