β-1, 3-galactosyltransferase 2 deficiency exacerbates brain injury after transient focal cerebral ischemia in mice

半影 医学 缺血 脑缺血 卷绕 脑损伤 细胞凋亡 内分泌学 内科学 神经科学 生物 生物化学 受体
作者
Mengjie Jia,Xue Yang,Tianhui Yang,Xinyang Deng,Jia Liang,Jing Bi,Peng Wang
出处
期刊:Brain Research Bulletin [Elsevier]
卷期号:169: 104-111 被引量:10
标识
DOI:10.1016/j.brainresbull.2021.01.010
摘要

Glycosyltransferases are enzymes that catalyze the formation of a variety of glycoconjugates. Glycoconjugates play vital roles in the nervous system. β-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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