GLAST-CreER^T2 mediated deletion of GDNF increases brain damage and exacerbates long-term stroke outcomes after focal ischemic stroke in mouse model.

ABSTRACT: Focal ischemic stroke (FIS) is a leading cause of human death. Glial scar formation largely caused by reactive astrogliosis in peri-infarct region (PIR) is the hallmark of FIS. Glial cell-derived neurotrophic factor (GDNF) was originally isolated from a rat glioma cell-line supernatant and is a potent survival neurotrophic factor. Here, using CreER^T2 -LoxP recombination technology, we generated inducible and astrocyte-specific GDNF conditional knockout (cKO), that is, GLAST-GDNF^-/- cKO mice to investigate the effect of reactive astrocytes (RAs)-derived GDNF on neuronal death, brain damage, oxidative stress and motor function recovery after photothrombosis (PT)-induced FIS. Under non-ischemic conditions, we found that adult GLAST-GDNF^-/- cKO mice exhibited s

SUBMITTER: Zhang N 

PROVIDER: S-EPMC8261898 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature