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 Blood, 15 March 2005, Vol. 105, No. 6, pp. 2343-2349.
Prepublished online as a Blood First Edition Paper on October 21, 2004; DOI 10.1182/blood-2004-08-3140.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

Mechanism by which H-2g, a glucose analog of blood group H antigen, mediates angiogenesis

Kui Zhu, Mohammed Asif Amin, Yuanyuan Zha, Lisa A. Harlow, and Alisa E. Koch

From the Department of Medicine, Northwestern University Feinberg School of Medicine and the Veterans Administration Chicago Healthcare System, Lakeside Division, Chicago, IL; the Division of Rheumatology, University of Michigan and the Veterans Administration Ann Arbor Healthcare System, Ann Arbor, MI.

The 4A11 antigen is a unique cytokine-inducible antigen up-regulated on rheumatoid arthritis (RA) synovial endothelial cells (ECs) compared with normal ECs. Previously, we showed that in soluble form, this antigen, Lewisy-6/H-5-2 (Ley/H) or its glucose analog, 2-fucosyl lactose (H-2g), induced the expression of EC intercellular adhesion molecule-1 (ICAM-1) and leukocyte-endothelial adhesion through the Janus kinase 2 (JAK2)–signal transducer and activator of transcription 3 (STAT3) pathway. Currently, we show that H-2g induces release of EC angiogenic basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), an effect inhibited by decoy nuclear factor {kappa}B (NF{kappa}B) oligodeoxynucleotide (ODN). JAK2 and phosphoinositide-3 kinase (PI3K) are 2 upstream kinases of NF{kappa}B activated by H-2g, as confirmed by an inhibitor of kappa B kinase (IKK{beta}) assay. In vitro, H-2g induces vascular sprouting in the rat aortic ring model, whereas blockade of JAK2, PI3K, or NF{kappa}B inhibits sprouting. Likewise, in the in vivo mouse Matrigel plug angiogenesis assay, chemical inhibitors and antisense or decoy ODNs of JAK2, PI3K, or NF{kappa}B decrease angiogenesis, confirming the importance of these pathways in H-2g–induced EC signaling. The critical role of Ley/H involvement in angiogenesis and its signaling pathways may provide new targets for therapy of diseases characterized by pathologic neovascularization.


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