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The Journal of Immunology, 2004, 173: 5801-5809.
Copyright © 2004 by The American Association of Immunologists

Crucial Role of Inhibitor of DNA Binding/Differentiation in the Vascular Endothelial Growth Factor-Induced Activation and Angiogenic Processes of Human Endothelial Cells1

Daisuke Sakurai*,¶, Naoyuki Tsuchiya2,*, Akihiro Yamaguchi{dagger}, Yurai Okaji{ddagger}, Nelson H. Tsuno§, Tetsuji Kobata, Koki Takahashi§ and Katsushi Tokunaga*

Departments of * Human Genetics, {dagger} Allergy and Rheumatology, {ddagger} Surgical Oncology, and § Transfusion Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan; and Division of Immunology, Institute for Medical Science, Dokkyo University School of Medicine, Tochigi, Japan

Angiogenesis plays a pivotal role in the aggressive proliferation of synovial cells in rheumatoid arthritis. We have previously reported the overexpression of inhibitor of DNA binding/differentiation (Id) in the endothelial cells within the synovial tissues of rheumatoid arthritis. In this study, we investigated the role of Id in inflammation and angiogenesis in an in vitro model using HUVECs. Vascular endothelial growth factor (VEGF) and TGF{beta} induced the expression of Id1 and Id3 in HUVECs. Forced expression of Id induced proliferative activity in HUVECs accompanied by down-regulation of p16INK4a. Overexpression of Id enhanced expression of ICAM-1 and E-selectin, and induced angiogenic processes such as transmigration, matrix metalloproteinase-2 and -9 expression, and tube formation. In contrast, knockdown of Id1 and Id3 with RNA interference abolished proliferation, activation, and angiogenic processes of HUVECs induced by VEGF. These results indicated that Id plays a crucial role in VEGF-induced signals of endothelial cells by causing activation and potentiation of angiogenic processes. Based on these findings, it was proposed that inhibition of expression and/or function of Id1 and Id3 may potentially be of therapeutic value for conditions associated with pathological angiogenesis.




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