Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7505
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dc.contributor.authorFrenis, Katie-
dc.contributor.authorHelmstädter, Johanna-
dc.contributor.authorRuan, Yue-
dc.contributor.authorSchramm, Eva-
dc.contributor.authorKalinovic, Sanela-
dc.contributor.authorKröller-Schön, Swenja-
dc.contributor.authorBayo Jimenez, Maria Teresa-
dc.contributor.authorHahad, Omar-
dc.contributor.authorOelze, Matthias-
dc.contributor.authorJiang, Subao-
dc.contributor.authorWenzel, Philip-
dc.contributor.authorSommer, Clemens J.-
dc.contributor.authorFrauenknecht, Katrin B. M.-
dc.contributor.authorWaisman, Ari-
dc.contributor.authorGericke, Adrian-
dc.contributor.authorDaiber, Andreas-
dc.contributor.authorMünzel, Thomas-
dc.contributor.authorSteven, Sebastian-
dc.date.accessioned2022-08-04T09:48:35Z-
dc.date.available2022-08-04T09:48:35Z-
dc.date.issued2021-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7519-
dc.description.abstractAircraft noise induces vascular and cerebral inflammation and oxidative stress causing hypertension and cardiovascular/cerebral dysfunction. With the present studies, we sought to determine the role of myeloid cells in the vascular vs. cerebral consequences of exposure to aircraft noise. Toxin-mediated ablation of lysozyme M+ (LysM+) myeloid cells was performed in LysMCreiDTR mice carrying a cre-inducible diphtheria toxin receptor. In the last 4d of toxin treatment, the animals were exposed to noise at maximum and mean sound pressure levels of 85 and 72 dB(A), respectively. Flow cytometry analysis revealed accumulation of CD45+, CD11b+, F4/80+, and Ly6G−Ly6C+ cells in the aortas of noise-exposed mice, which was prevented by LysM+ cell ablation in the periphery, whereas brain infiltrates were even exacerbated upon ablation. Aircraft noise-induced increases in blood pressure and endothelial dysfunction of the aorta and retinal/mesenteric arterioles were almost completely normalized by ablation. Correspondingly, reactive oxygen species in the aorta, heart, and retinal/mesenteric vessels were attenuated in ablated noise-exposed mice, while microglial activation and abundance in the brain was greatly increased. Expression of phagocytic NADPH oxidase (NOX-2) and vascular cell adhesion molecule-1 (VCAM-1) mRNA in the aorta was reduced, while NFκB signaling appeared to be activated in the brain upon ablation. In sum, we show dissociation of cerebral and peripheral inflammatory reactions in response to aircraft noise after LysM+ cell ablation, wherein peripheral myeloid inflammatory cells represent a dominant part of the pathomechanism for noise stress-induced cardiovascular effects and their central nervous counterparts, microglia, as key mediators in stress responses.en_GB
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleAblation of lysozyme M-positive cells prevents aircraft noise-induced vascular damage without improving cerebral side effectsen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7505-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleBasic research in cardiologyde
jgu.journal.volume116de
jgu.pages.alternative31de
jgu.publisher.year2021-
jgu.publisher.nameSteinkopffde
jgu.publisher.placeDarmstadt u.a.de
jgu.publisher.issn1435-1803de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.1007/s00395-021-00869-5de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:JGU-Publikationen

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