ß-1, 3-galactosyltransferase 2 deficiency exacerbates brain injury after transient focal cerebral ischemia in mice.
Brain Res Bull
; 169: 104-111, 2021 04.
Article
em En
| MEDLINE
| ID: mdl-33482286
ABSTRACT
Glycosyltransferases are enzymes that catalyze the formation of a variety of glycoconjugates. Glycoconjugates play vital roles in the nervous system. ß-1, 3-Galactosyltransferase 2 (B3galt2) is one of the major types of glycosyltransferases, which has not been reported in ischemia induced-brain injury. The purpose of this study was to explore the role of B3galt2 exerts and its underlying mechanism in cerebral ischemia in mice. Wild-type (WT) and heterozygous B3galt2 knockout (B3galt2-/+) mice were subjected to 90 min transient focal cerebral ischemia by middle cerebral artery occlusion (MCAO). The brain samples were analyzed at 24 h after reperfusion. The B3galt2 level in the peri-infarct penumbra was quantified. The cerebral infarct volume, neurological deficits, apoptosis and the levels of Reelin and Dab1 were assessed. Compared with control mice, B3galt2-/+ mice not only showed severe brain damage, neurologic functional deficits, but also showed severe neuronal apoptosis in the cortical penumbra after ischemia/reperfusion (I/R). The Caspase-3 activity was increased and the levels of Reelin and Dab1 were decreased in B3galt2-/+ mice. Recombinant human Reelin (rh-Reelin) administered intracerebroventricularly before MCAO significantly reduced infarct volume, and prevented neuronal loss in B3galt2-/+ mice after I/R. Our results suggest B3galt2 deficiency exacerbates ischemic brain damage in acute ischemic stroke in mice, and this was reversed by giving rh-Reelin. B3galt2 might play a beneficial role for neurons survival in the penumbra through modulation of Reelin pathway.
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Texto completo:
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Encéfalo
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Isquemia Encefálica
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Apoptose
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Galactosiltransferases
Limite:
Animals
Idioma:
En
Revista:
Brain Res Bull
Ano de publicação:
2021
Tipo de documento:
Article
País de afiliação:
China