TY - JOUR
T1 - 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
AU - Kurushima, H.
AU - Ohno, M.
AU - Miura, T.
AU - Nakamura, T. Y.
AU - Horie, H.
AU - Kadoya, T.
AU - Ooboshi, H.
AU - Kitazono, T.
AU - Ibayashi, S.
AU - Iida, M.
AU - Nakabeppu, Yusaku
N1 - Funding Information:
We thank Drs. Kunihiko Sakumi, Daisuke Tsuchimoto and Masato Furuichi for their helpful discussions, Setsuko Kitamura and Keiko Aiura for their technical assistance and Dr. B Quinn for comments on the manuscript. This work was supported by grants from CREST, Japan Science and Technology Agency, the Ministry of Education, Culture, Sports, Science, and Technology of Japan (Grant 16012248) and the Japan Society for the Promotion of Science (Grants: 15590347 and 16390119).
PY - 2005/8
Y1 - 2005/8
N2 - Transient forebrain ischemia causes selective induction of ΔFosB, 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 β-galactoside sugar-binding lectin. The adenovirus-mediated expression of FOSB or ΔFosB induced expression of nestin, glial fibrillary acidic protein and galectin-1 in rat embryonic cortical cells. ΔFosB-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 ΔFosB expression in the survivors enhanced the MAP2 expression. The expression of ΔFosB in cells within the ventricle wall of the rat brain also resulted in an elevated expression of nestin. We therefore conclude that ΔFosB can promote the proliferation of quiescent neuronal precursor cells, thus enhancing neurogenesis after transient forebrain ischemia.
AB - Transient forebrain ischemia causes selective induction of ΔFosB, 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 β-galactoside sugar-binding lectin. The adenovirus-mediated expression of FOSB or ΔFosB induced expression of nestin, glial fibrillary acidic protein and galectin-1 in rat embryonic cortical cells. ΔFosB-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 ΔFosB expression in the survivors enhanced the MAP2 expression. The expression of ΔFosB in cells within the ventricle wall of the rat brain also resulted in an elevated expression of nestin. We therefore conclude that ΔFosB can promote the proliferation of quiescent neuronal precursor cells, thus enhancing neurogenesis after transient forebrain ischemia.
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U2 - 10.1038/sj.cdd.4401648
DO - 10.1038/sj.cdd.4401648
M3 - Article
C2 - 15861185
AN - SCOPUS:23044516204
VL - 12
SP - 1078
EP - 1096
JO - Cell Death and Differentiation
JF - Cell Death and Differentiation
SN - 1350-9047
IS - 8
ER -