title: TGF-beta-induced protein beta ig-h3 is upregulated by high glucose in vascular smooth muscle cells.
abstract: TGF-beta-induced gene-h3 (beta ig-h3) is an adhesive molecule that interacts with integrins. Because TGF-beta plays an important role in diabetic complications and beta ig-h3 serves as a cell substrate, we hypothesized that diabetic conditions might increase beta ig-h3 synthesis in vascular smooth muscle cells (VSMCs), which may subsequently contribute to the pathogenesis of diabetic angiopathy. The concentrations of beta ig-h3 and TGF-beta were measured in conditioned media using an enzyme-linked immunosorbent assay. An immunohistochemical study showed that beta ig-h3 was expressed in the VSMCs and the matrix of rat aortas. TGF-beta stimulated beta ig-h3 production, and high glucose induced beta ig-h3 as well as TGF-beta production in the VSMCs. The high glucose-induced beta ig-h3 expression was almost entirely blocked by an anti-TGF-beta antibody. beta ig-h3 protein mediated the adhesion, spreading, migration, and proliferation of rat VSMCs. These results suggest that the high glucose-induced beta ig-h3 in VSMCs regulates VSMC functions and may play an important role in diabetic angiopathy.
authors.affiliation: Department of Internal Medicine, Kyungpook National University, School of Medicine, Daegu, 700-422, Republic of Korea.
authors.forename: Sung-Woo
authors.initials: SW
authors.lastname: Ha
authors.forename: Jong-Sup
authors.initials: JS
authors.lastname: Bae
authors.forename: Hye-Jin
authors.initials: HJ
authors.lastname: Yeo
authors.forename: Suk-Hee
authors.initials: SH
authors.lastname: Lee
authors.forename: Je-Yong
authors.initials: JY
authors.lastname: Choi
authors.forename: Yoon-Kyung
authors.initials: YK
authors.lastname: Sohn
authors.forename: Jung-Guk
authors.initials: JG
authors.lastname: Kim
authors.forename: In-San
authors.initials: IS
authors.lastname: Kim
authors.forename: Bo-Wan
authors.initials: BW
authors.lastname: Kim
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism; D002448:Cell Adhesion; D002455:Cell Division; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D003925:Diabetic Angiopathies / Q000209:etiology / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D006133:Growth Substances / Q000494:pharmacology; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D008297:Male; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000378:metabolism; D010455:Peptides; D051381:Rats; D017207:Rats, Sprague-Dawley; D016212:Transforming Growth Factor beta / Q000032:analysis / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000099222:betaIG-H3 Protein
chemical_list: D016326:Extracellular Matrix Proteins; D005947:Glucose; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D010455:Peptides; D016212:Transforming Growth Factor beta; D000099222:betaIG-H3 Protein; C429104:SPON1 protein, human; C498955:Spon1 protein, rat