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Bardon, Andreas Garcia
Coronel-Castello, Shila P.
Krämer, Tobias J.
Steckelings, Ulrike Muscha
Thal, Serge C.
|Title:||AT2 activation does not influence brain damage in the early phase after experimental traumatic brain injury in male mice|
|Online publication date:||10-Feb-2023|
|Year of first publication:||2022|
|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.|
610 Medical sciences
|Institution:||Johannes Gutenberg-Universität Mainz|
|Department:||FB 04 Medizin|
|Document type specification:||Scientific article|
|Information on rights of use:||https://creativecommons.org/licenses/by/4.0/|
|Pages or article number:||14280|
|Publisher:||Macmillan Publishers Limited, part of Springer Nature|
|Appears in collections:||DFG-491381577-G|
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