Gutenberg Open Science: AT2 activation does not influence brain damage in the early phase after experimental traumatic brain injury in male mice

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-8673

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DC Field	Value	Language
dc.contributor.author	Timaru-Kast, Ralph	-
dc.contributor.author	Bardon, Andreas Garcia	-
dc.contributor.author	Luh, Clara	-
dc.contributor.author	Coronel-Castello, Shila P.	-
dc.contributor.author	Songarj, Phuripong	-
dc.contributor.author	Griemert, Eva-Verena	-
dc.contributor.author	Krämer, Tobias J.	-
dc.contributor.author	Sebastiani, Anne	-
dc.contributor.author	Steckelings, Ulrike Muscha	-
dc.contributor.author	Thal, Serge C.	-
dc.date.accessioned	2023-02-10T10:59:10Z	-
dc.date.available	2023-02-10T10:59:10Z	-
dc.date.issued	2022	-
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/8689	-
dc.description.abstract	Antagonism of the angiotensin II type 1 receptor (AT1) improves neurological function and reduces brain damage after experimental traumatic brain injury (TBI), which may be partly a result of enhanced indirect angiotensin II type 2 receptor (AT2) stimulation. AT2 stimulation was demonstrated to be neuroprotective via anti-inflammatory, vasodilatory, and neuroregenerative mechanisms in experimental cerebral pathology models. We recently demonstrated an upregulation of AT2 after TBI suggesting a protective mechanism. The present study investigated the effect of post-traumatic (5 days after TBI) AT2 activation via high and low doses of a selective AT2 agonist, compound 21 (C21), compared to vehicle-treated controls. No differences in the extent of the TBI-induced lesions were found between both doses of C21 and the controls. We then tested AT2-knockdown animals for secondary brain damage after experimental TBI. Lesion volume and neurological outcomes in AT2-deficient mice were similar to those in wild-type control mice at both 24 h and 5 days post-trauma. Thus, in contrast to AT1 antagonism, AT2 modulation does not influence the initial pathophysiological mechanisms of TBI in the first 5 days after the insult, indicating that AT2 plays only a minor role in the early phase following trauma-induced brain damage.	en_GB
dc.description.sponsorship	Gefördert durch die Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 491381577	de
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	AT2 activation does not influence brain damage in the early phase after experimental traumatic brain injury in male mice	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-8673	-
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	12	de
jgu.pages.alternative	14280	de
jgu.publisher.year	2022	-
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/s41598-022-18338-x	de
jgu.organisation.ror	https://ror.org/023b0x485	-
jgu.subject.dfg	Lebenswissenschaften	de
Appears in collections:	DFG-491381577-G

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