rdf:type |
|
lifeskim:mentions |
umls-concept:C0006104,
umls-concept:C0017262,
umls-concept:C0022116,
umls-concept:C0085140,
umls-concept:C0185117,
umls-concept:C0205217,
umls-concept:C0205263,
umls-concept:C0205374,
umls-concept:C0252527,
umls-concept:C0598958,
umls-concept:C0814002,
umls-concept:C2911684
|
pubmed:issue |
8
|
pubmed:dateCreated |
2005-7-14
|
pubmed:abstractText |
Transient forebrain ischemia causes selective induction of DeltaFosB, 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 DeltaFosB induced expression of nestin, glial fibrillary acidic protein and galectin-1 in rat embryonic cortical cells. DeltaFosB-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 DeltaFosB expression in the survivors enhanced the MAP2 expression. The expression of DeltaFosB in cells within the ventricle wall of the rat brain also resulted in an elevated expression of nestin. We therefore conclude that DeltaFosB can promote the proliferation of quiescent neuronal precursor cells, thus enhancing neurogenesis after transient forebrain ischemia.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
1350-9047
|
pubmed:author |
pubmed-author:HorieHH,
pubmed-author:IbayashiSS,
pubmed-author:IidaMM,
pubmed-author:KadoyaTT,
pubmed-author:KitazonoTT,
pubmed-author:KurushimaHH,
pubmed-author:MiuraTT,
pubmed-author:NakabeppuYY,
pubmed-author:NakamuraT YTY,
pubmed-author:OhnoMM,
pubmed-author:OoboshiHH
|
pubmed:issnType |
Print
|
pubmed:volume |
12
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1078-96
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:15861185-Adenoviridae,
pubmed-meshheading:15861185-Animals,
pubmed-meshheading:15861185-Brain,
pubmed-meshheading:15861185-Cells, Cultured,
pubmed-meshheading:15861185-Cerebral Cortex,
pubmed-meshheading:15861185-Embryo, Mammalian,
pubmed-meshheading:15861185-Galectin 1,
pubmed-meshheading:15861185-Glial Fibrillary Acidic Protein,
pubmed-meshheading:15861185-Immunohistochemistry,
pubmed-meshheading:15861185-Intermediate Filament Proteins,
pubmed-meshheading:15861185-Ischemic Attack, Transient,
pubmed-meshheading:15861185-Male,
pubmed-meshheading:15861185-Mice,
pubmed-meshheading:15861185-Microscopy, Confocal,
pubmed-meshheading:15861185-Microscopy, Fluorescence,
pubmed-meshheading:15861185-Nerve Tissue Proteins,
pubmed-meshheading:15861185-Neurons,
pubmed-meshheading:15861185-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:15861185-Rabbits,
pubmed-meshheading:15861185-Rats,
pubmed-meshheading:15861185-Rats, Inbred SHR,
pubmed-meshheading:15861185-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15861185-Transcription Factors
|
pubmed:year |
2005
|
pubmed:articleTitle |
Selective induction of DeltaFosB in the brain after transient forebrain ischemia accompanied by an increased expression of galectin-1, and the implication of DeltaFosB and galectin-1 in neuroprotection and neurogenesis.
|
pubmed:affiliation |
Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|