TGF-β-induced protein βig-h3 is upregulated by high glucose in vascular smooth muscle cells

✍ Scribed by Sung-Woo Ha; Jong-Sup Bae; Hye-Jin Yeo; Suk-Hee Lee; Je-Yong Choi; Yoon-Kyung Sohn; Jung-Guk Kim; In-San Kim; Bo-Wan Kim

• Publisher: John Wiley and Sons
• Year: 2003
• Tongue: English
• Weight: 329 KB
• Volume: 88
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.10374

✦ Synopsis

Abstract

TGF‐β‐induced gene‐h3 (βig‐h3) is an adhesive molecule that interacts with integrins. Because TGF‐β plays an important role in diabetic complications and βig‐h3 serves as a cell substrate, we hypothesized that diabetic conditions might increase βig‐h3 synthesis in vascular smooth muscle cells (VSMCs), which may subsequently contribute to the pathogenesis of diabetic angiopathy. The concentrations of βig‐h3 and TGF‐β were measured in conditioned media using an enzyme‐linked immunosorbent assay. An immunohistochemical study showed that βig‐h3 was expressed in the VSMCs and the matrix of rat aortas. TGF‐β stimulated βig‐h3 production, and high glucose induced βig‐h3 as well as TGF‐β production in the VSMCs. The high glucose‐induced βig‐h3 expression was almost entirely blocked by an anti‐TGF‐β antibody. βig‐h3 protein mediated the adhesion, spreading, migration, and proliferation of rat VSMCs. These results suggest that the high glucose‐induced βig‐h3 in VSMCs regulates VSMC functions and may play an important role in diabetic angiopathy. © 2002 Wiley‐Liss, Inc.