Angiotensin receptor type 2 activation induces neuroprotection and neurogenesis after traumatic brain injury.

ABSTRACT: Angiotensin II receptor type 2 (AT(2)) agonists have been shown to limit brain ischemic insult and to improve its outcome. The activation of AT(2) was also linked to induced neuronal proliferation and differentiation in vitro. In this study, we examined the therapeutic potential of AT(2) activation following traumatic brain injury (TBI) in mice, a brain pathology that displays ischemia-like secondary damages. The AT(2) agonist CGP42112A was continuously infused immediately after closed head injury (CHI) for 3 days. We have followed the functional recovery of the injured mice for 35 days post-CHI, and evaluated cognitive function, lesion volume, molecular signaling, and neurogenesis at different time points after the impact. We found dose-dependent improvement in functional recovery and cog

SUBMITTER: Umschweif G 

PROVIDER: S-EPMC4121449 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature