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TGF‐β‐induced protein βig‐h3 is upregulated by high glucose in vascular smooth muscle cells
Author(s) -
Ha SungWoo,
Bae JongSup,
Yeo HyeJin,
Lee SukHee,
Choi JeYong,
Sohn YoonKyung,
Kim JungGuk,
Kim InSan,
Kim BoWan
Publication year - 2002
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10374
Subject(s) - vascular smooth muscle , downregulation and upregulation , medicine , immunoglobulin superfamily , angiopathy , antibody , endocrinology , integrin , transforming growth factor , chemistry , microbiology and biotechnology , cell adhesion molecule , biology , receptor , smooth muscle , immunology , diabetes mellitus , gene , biochemistry
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.