title: Identification of a novel gene, OASIS, which encodes for a putative CREB/ATF family transcription factor in the long-term cultured astrocytes and gliotic tissue.
abstract: Gliosis is a characteristic response of astrocytes to inflammation and trauma of the central nervous system (CNS). To study the mechanisms underlying gliosis, we performed differential display screening for genes specifically induced in long-term cultured astrocytes used as an in vitro gliosis model. We identified and characterized a gene (named OASIS, for old astrocyte specifically-induced substance) expressed in long-term cultured mouse astrocytes, or 'old astrocytes (OA)'. The OASIS gene encoded a putative transcription factor belonging to the cyclic AMP responsive element binding protein/activating transcription factor (CREB/ATF) gene family, with homology to box B-binding factor-2 (BBF-2), a Drosophila transcription factor. Its expression was developmentally regulated; OASIS mRNA was primarily expressed in the salivary gland and cartilage in the mouse embryo and it was transiently upregulated in the brain during postnatal two weeks. The expression became weaker in the adult brain. We also demonstrated that an expression of the OASIS mRNA was induced in response to the cryo-injury of the mouse cerebral cortex. The distribution pattern of the OASIS-positive cells in the injured cortex was very similar to that of the glial fibrillary acidic protein (GFAP)-positive cells. These results suggest that OASIS protein may play a role in gliotic events.
authors.affiliation: Department of Cell Science, Institute of Biomedical Sciences, 1 Hikarigaoka, Fukushima City, Fukushima 960-1295, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Honma
authors.forename: K
authors.initials: K
authors.lastname: Kanazawa
authors.forename: T
authors.initials: T
authors.lastname: Mori
authors.forename: Y
authors.initials: Y
authors.lastname: Tanno
authors.forename: M
authors.initials: M
authors.lastname: Tojo
authors.forename: H
authors.initials: H
authors.lastname: Kiyosawa
authors.forename: J
authors.initials: J
authors.lastname: Takeda
authors.forename: T
authors.initials: T
authors.lastname: Nikaido
authors.forename: T
authors.initials: T
authors.lastname: Tsukamoto
authors.forename: S
authors.initials: S
authors.lastname: Yokoya
authors.forename: A
authors.initials: A
authors.lastname: Wanaka
mesh_terms: D051696:Activating Transcription Factors; D000367:Age Factors; D000818:Animals; D001253:Astrocytes / Q000737:chemistry* / Q000502:physiology*; D001798:Blood Proteins / Q000235:genetics*; D015152:Blotting, Northern; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology; D003001:Cloning, Molecular; D017362:Cyclic AMP Response Element-Binding Protein / Q000235:genetics*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D005911:Gliosis / Q000276:immunology; D017403:In Situ Hybridization; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D008969:Molecular Sequence Data; D009419:Nerve Tissue Proteins; D009443:Neuritis / Q000235:genetics / Q000276:immunology; D012333:RNA, Messenger / Q000032:analysis; D017386:Sequence Homology, Amino Acid; D014157:Transcription Factors / Q000235:genetics*
chemical_list: D051696:Activating Transcription Factors; D001798:Blood Proteins; C119923:Creb3l1 protein, mouse; D017362:Cyclic AMP Response Element-Binding Protein; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D014157:Transcription Factors