Gutenberg Open Science: AT 1 inhibition mediated neuroprotection after experimental traumatic brain injury is dependent on neutrophils in male mice

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-9967

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DC Field	Value	Language
dc.contributor.author	Timaru-Kast, Ralph	-
dc.contributor.author	Coronel-Castello, Shila P.	-
dc.contributor.author	Krämer, Tobias J.	-
dc.contributor.author	Hugonnet, André V.	-
dc.contributor.author	Schäfer, Michael K. E.	-
dc.contributor.author	Sebastiani, Anne	-
dc.contributor.author	Thal, Serge C.	-
dc.date.accessioned	2024-01-24T11:28:45Z	-
dc.date.available	2024-01-24T11:28:45Z	-
dc.date.issued	2023	-
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/9985	-
dc.description.abstract	After traumatic brain injury (TBI) cerebral inflammation with invasion of neutrophils and lymphocytes is a crucial factor in the process of secondary brain damage. In TBI the intrinsic renin-angiotensin system is an important mediator of cerebral inflammation, as inhibition of the angiotensin II receptor type 1 (AT1) reduces secondary brain damage and the invasion of neutrophil granulocytes into injured cerebral tissue. The current study explored the involvement of immune cells in neuroprotection mediated by AT1 inhibition following experimental TBI. Four different cohorts of male mice were examined, investigating the effects of neutropenia (anti-Ly6G antibody mediated neutrophil depletion; C57BL/6), lymphopenia (RAG1 deficiency, RAG1−/−), and their combination with candesartan-mediated AT1 inhibition. The present results showed that reduction of neutrophils and lymphocytes, as well as AT1 inhibition in wild type and RAG1−/− mice, reduced brain damage and neuroinflammation after TBI. However, in neutropenic mice, candesartan did not have an effect. Interestingly, AT1 inhibition was found to be neuroprotective in RAG1−/− mice but not in neutropenic mice. The findings suggest that AT1 inhibition may exert neuroprotection by reducing the inflammation caused by neutrophils, ultimately leading to a decrease in their invasion into cerebral tissue.	en_GB
dc.language.iso	eng	de
dc.rights	CC BY	*
dc.rights.uri	https://creativecommons.org/licenses/by/4.0/	*
dc.subject.ddc	610 Medizin	de_DE
dc.subject.ddc	610 Medical sciences	en_GB
dc.title	AT 1 inhibition mediated neuroprotection after experimental traumatic brain injury is dependent on neutrophils in male mice	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-9967	-
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	Scientific reports	de
jgu.journal.volume	13	de
jgu.pages.alternative	7413	de
jgu.publisher.year	2023	-
jgu.publisher.name	Macmillan Publishers Limited, part of Springer Nature	de
jgu.publisher.place	London	de
jgu.publisher.issn	2045-2322	de
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	610	de
jgu.publisher.doi	10.1038/s41598-023-33797-6	de
jgu.organisation.ror	https://ror.org/023b0x485	-
Appears in collections:	DFG-491381577-G

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