Search results for: VEGI TNFSF 15, human recombinant
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Vascular endothelial growth inhibitor (VEGI), an endogenous negative regulator of angiogenesis.
Vascular endothelial growth inhibitor (VEGI; TNFSF-15) is a new member of the tumor necrosis factor family. VEGI is predominantly an endothelial cell-specific gene, and recombinant VEGI is a potent inhibitor of endothelial cell proliferation, angiogenesis and tumor growth. VEGI exerts two activities on endothelial cells: early G1 arrest of G0/G1-cells responding to growth stimuli, and programmed death of proliferating cells. These activities are highly specific to endothelial cells. There are three VEGI isoforms identified thus far. One of the isoforms, VEGI-251, is a secreted protein. The gene products apparently play a role in normal vasculature, as the transcripts are found in normal adult tissues and some fetal tissues. VEGI gene expression is subject to regulation by inflammatory cytokines. VEGI is also able to regulate the expression of several important genes involved in angiogenesis. These findings are consistent with the view that VEGI functions as an autocrine cytokine to inhibit angiogenesis and stabilize the vasculature.Linda J Metheny-Barlow, Lu-Yuan Li
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Involvement of TL1A and DR3 in induction of pro-inflammatory cytokines and matrix metalloproteinase-9 in atherogenesis.
TL1A (VEGI/TNFSF15) is the ligand for DR3 (TNFRSF12) and is a newly identified member of the tumor necrosis factor superfamily (TNFSF). Previously, DR3 has been shown to have a role in atherogenesis through stimulation of matrix degrading enzymes including matrix metalloproteinase (MMP)-9. Immunohistochemical staining of human carotid atherosclerotic plaques revealed a high-level expression of TL1A in regions rich in macrophage/foam cells. To investigate the role of TL1A and DR3 in the functioning of macrophage/foam cells in relation to atherogenesis, we have analyzed cellular events mediated by TL1A and DR3 in a human macrophage-like cell line, THP-1. Treatment of THP-1 cells with immobilized anti-DR3 monoclonal antibody in combination with IFN-gamma caused induction of pro-atherogenic cytokines/chemokines such as TNF-alpha, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-8. Treatment of THP-1 cells with recombinant TL1A in combination with IFN-gamma also caused induction of MMP-9 and IL-8. Furthermore, the expression of DR3 in peripheral blood monocytes was induced after atherogenic stimulation. These data suggest that TL1A and DR3 is involved in atherosclerosis via the induction of pro-inflammatory cytokines/chemokines and decreasing plaque stability by inducing extracellular matrix degrading enzymes.Yoon-Joong Kang, Won-Jung Kim, Hyung-Uk Bae, Dong-Ik Kim, Yong Bok Park, Jeong-Euy Park, Byoung S Kwon, Won-Ha Lee