title: Induction of TGF-beta-inducible gene-h3 (betaig-h3) by TGF-beta1 in astrocytes: implications for astrocyte response to brain injury.
abstract: Transforming growth factor (TGF)-beta-inducible gene-h3 (betaig-h3) product is a secreted protein that is induced by TGF-beta in several cell types and implicated in various tissue pathologies. The aims of this study were to determine the effect of TGF-beta1 on betaig-h3 expression in cultured astrocytes and to examine whether betaig-h3 is expressed in the brain after traumatic injury. The results showed that betaig-h3 mRNA and protein increased in response to TGF-beta1 in U87 human astrocytoma cells and mouse cortical astrocytes. Treatment with other cytokines, including tumor necrosis factor-alpha and fibroblast growth factor-2, did not enhance the expression of betaig-h3 in astrocytes. betaig-h3 was significantly expressed in reactive astrocytes at the site of a stab wound in the cerebral cortex of adult rats. These results provide an insight into understanding a novel role for betaig-h3 protein in the response of astrocytes to brain injury.
authors.affiliation: Graduate School of East-West Medical Science, Kyung Hee University, Yong-In 449-701, South Korea.
authors.forename: Su-Jin
authors.initials: SJ
authors.lastname: Yun
authors.forename: Mi-Ok
authors.initials: MO
authors.lastname: Kim
authors.forename: Sung Ok
authors.initials: SO
authors.lastname: Kim
authors.forename: Jiho
authors.initials: J
authors.lastname: Park
authors.forename: Yunhee K
authors.initials: YK
authors.lastname: Kwon
authors.forename: In-San
authors.initials: IS
authors.lastname: Kim
authors.forename: Eunjoo H
authors.initials: EH
authors.lastname: Lee
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism*; D001930:Brain Injuries / Q000235:genetics / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D016326:Extracellular Matrix Proteins; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D016212:Transforming Growth Factor beta / Q000378:metabolism* / Q000494:pharmacology; D053773:Transforming Growth Factor beta1; D014407:Tumor Cells, Cultured; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology; D014945:Wound Healing / Q000187:drug effects / Q000235:genetics*; D000099222:betaIG-H3 Protein
chemical_list: D016326:Extracellular Matrix Proteins; D005904:Glial Fibrillary Acidic Protein; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D000099222:betaIG-H3 Protein; C508960:TGFB1 protein, human; C508961:Tgfb1 protein, mouse; C508962:Tgfb1 protein, rat