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

被引：21
作者：
Ha, SW
Bae, JS
Yeo, HJ
Lee, SH
Choi, JY
Sohn, YK
Kim, JG
Kim, IS [1 ]
Kim, BW
机构：
[1] Kyungpook Natl Univ, Sch Med, Dept Internal Med, Taegu 700422, South Korea
[2] Kyungpook Natl Univ, Sch Med, Dept Biochem, Taegu 700422, South Korea
[3] Kyungpook Natl Univ, Sch Med, Dept Pathol, Taegu 700422, South Korea
来源：
JOURNAL OF CELLULAR BIOCHEMISTRY | 2003年 / 88卷 / 04期
关键词：
beta ig-h3; vascular smooth muscle cells; high glucose; TGF-beta; diabetic angiopathy;
D O I：
10.1002/jcb.10374
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
TGF-beta-induced gene-h3 (betaig-H) is an adhesive molecule that interacts with integrins. Because TGF-beta plays an important role in diabetic complications and betaig-h3 serves as a cell substrate, we hypothesized that diabetic conditions might increase betaig-h3 synthesis in vascular smooth muscle cells (VSMCs), which may subsequently contribute to the pathogenesis of diabetic angiopathy. The concentrations of betaig-h3 and TGF-beta were measured in conditioned media using an enzyme-linked immunosorbent assay. An immunohistochemical study showed that betaig-h3 was expressed in the VSMCs and the matrix of rat aortas. TGF-beta stimulated betaig-h3 production, and high glucose induced betaig-h3 as well as TGF-beta production in the VSMCs. The high glucose-induced betaig-h3 expression was almost entirely blocked by an anti-TGF-beta antibody. betaig-h3 protein mediated the adhesion, spreading, migration, and proliferation of rat VSMCs. These results suggest that the high glucose-induced betaig-h3 in VSMCs regulates VSMC functions and may play an important role in diabetic angiopathy.
引用
收藏
页码：774 / 782
页数：9
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