TGF-beta-induced protein beta ig-h3 is upregulated by high glucose in vascular smooth muscle cells |
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| Authors: | Ha Sung-Woo Bae Jong-Sup Yeo Hye-Jin Lee Suk-Hee Choi Je-Yong Sohn Yoon-Kyung Kim Jung-Guk Kim In-San Kim Bo-Wan |
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| Affiliation: | Department of Internal Medicine, Kyungpook National University, School of Medicine, Daegu, 700-422, Republic of Korea. |
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| 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. |
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| Keywords: | βig‐h3 vascular smooth muscle cells high glucose TGF‐β diabetic angiopathy |
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