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Nuclear Factor B Dependency of Platelet-activating Factor-induced Angiogenesis¹

Department of Biological Sciences, The Institute of Basic Sciences [H-M. K., K. H. S., S-J. H., S-Y. I], Research Institute of Medical Science [K. Y. A.], Chonnam National University, Kwangju 500-757; National Creative Research Initiatives Center for Endothelial Cells, Department of Life Science, Pohang University of Science and Technology, Pohang 790-784 [G. Y. K.]; Department of Immunology and Institute for Medical Sciences, Chonbuk National University Medical School, Chonju 561-756 [I-H. C., H-K. L.]; and Department of Food Environment and Health, Kwangju Women’s University, Kwangju 500-757 [M. S. R.], Republic of Korea

This study investigated the mechanisms of platelet-activating factor (PAF)-induced angiogenesis in a mouse model of Matrigel implantation. PAF induced a dose- and time-dependent angiogenic response. Inhibitors of nuclear factor (NF) B expression or action, including antisense oligonucleotides to the p65 subunit of NFB (p65 antisense) and antioxidants such as -tocopherol and N-acetyl-L-cysteine, significantly reduced PAF-induced angiogenesis. In human umbilical vein endothelial cells, PAF-induced mRNA expression and protein synthesis of various NFB-dependent angiogenic factors, such as tumor necrosis factor-, interleukin-1, basic fibroblast growth factor, and vascular endothelial growth factor (VEGF). The PAF-induced expression of the above mentioned factors was inhibited by p65 antisense or antioxidants. A significant inhibition of the angiogenic effect of PAF was achieved by anti-VEGF antibodies or soluble VEGF receptors such as KDR and flt-1 but not by antibodies against tumor necrosis factor-, interleukin-1, or basic fibroblast growth factor. These data indicate that PAF enhances angiogenesis through inducing NFB activation, which in turn promotes the production of angiogenic factors such as VEGF.

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