Selective induction of ΔFosB in the brain after transient forebrain ischemia accompanied by an increased expression of galectin-1, and the implication of ΔFosB and galectin-1 in neuroprotection and neurogenesis
Selective induction of ΔFosB in the brain after transient forebrain ischemia accompanied by an increased expression of galectin-1, and the implication of ΔFosB and galectin-1 in neuroprotection and neurogenesis
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DOI：
10.1038/sj.cdd.4401648
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发表时间：
2005-08-01
影响因子：
12.4
通讯作者：
Nakabeppu, Y
中科院分区：
文献类型：
--
作者：
Kurushima, H;Ohno, M;Nakabeppu, Y
短暂性前脑缺血导致在神经发生之前在大鼠脑中心室壁内的细胞或齿状回中的细胞中选择性诱导Delta FosB（AP-1（激活蛋白-1）亚基），随后诱导巢蛋白（神经元前体细胞的标记物）或半乳糖凝集素-1（β-半乳糖苷糖结合凝集素）。腺病毒介导的FosB或Delta FosB的表达诱导大鼠胚胎皮层细胞表达巢蛋白、胶质细胞酸性蛋白和半乳糖凝集素1。与对照或FosB表达细胞相比，Δ FosB表达细胞在撤除B27补充物后表现出显著更高的存活和增殖。存活者中Delta FosB表达的下降增强了MAP 2的表达。大鼠脑室壁内细胞中Delta FosB的表达也导致巢蛋白表达升高。因此，我们得出结论，三角洲FosB可以促进静止的神经元前体细胞的增殖，从而增强短暂前脑缺血后的神经发生。
Transient forebrain ischemia causes selective induction of Delta FosB, an AP-1 (activator protein-1) subunit, in cells within the ventricle wall or those in the dentate gyrus in the rat brain prior to neurogenesis, followed by induction of nestin, a marker for neuronal precursor cells, or galectin-1, a beta-galactoside sugar-binding lectin. The adenovirus-mediated expression of FosB or Delta FosB induced expression of nestin, glial fibrillary acidic protein and galectin-1 in rat embryonic cortical cells. Delta FosB-expressing cells exhibited a significantly higher survival and proliferation after the withdrawal of B27 supplement than the control or FosB-expressing cells. The decline in the Delta FosB expression in the survivors enhanced the MAP2 expression. The expression of Delta FosB in cells within the ventricle wall of the rat brain also resulted in an elevated expression of nestin. We therefore conclude that Delta FosB can promote the proliferation of quiescent neuronal precursor cells, thus enhancing neurogenesis after transient forebrain ischemia.