MONOCYTE TETHERING BY P-SELECTIN REGULATES MONOCYTE CHEMOTACTIC PROTEIN-1 AND TUMOR-NECROSIS-FACTOR-ALPHA SECRETION - SIGNAL INTEGRATION AND NF-KAPPA-B TRANSLOCATION
MONOCYTE TETHERING BY P-SELECTIN REGULATES MONOCYTE CHEMOTACTIC PROTEIN-1 AND TUMOR-NECROSIS-FACTOR-ALPHA SECRETION - SIGNAL INTEGRATION AND NF-KAPPA-B TRANSLOCATION
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DOI：
10.1172/jci117921
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发表时间：
1995-05-01
影响因子：
15.9
通讯作者：
ZIMMERMAN, GA
中科院分区：
文献类型：
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作者：
WEYRICH, AS;MCINTYRE, TM;ZIMMERMAN, GA
Adhesion molecules that tether circulating leukocytes to endothelial cells may also transduce or modulate outside-in signals for cellular activation, providing an initial regulatory point in the inflammatory response. Adhesion of human monocytes to P-selectin, the most rapidly expressed endothelial tethering factor, increased the secretion of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) by the leukocytes when they were stimulated with platelet-activating factor. Increased cytokine secretion was specifically inhibited by G1, an anti-P-selectin mAb that prevents P-selectin from binding to its ligand (P-selectin glycoprotein ligand-1) on myeloid cells. Moreover, tethering by P-selectin specifically enhanced nuclear translocation of nuclear factor-kappa B (NF-kappa B), a transcription factor required for expression of MCP-1, TIVF-alpha, and other immediate-early genes. These results demonstrate that P-selectin, through its ligands on monocytes, may locally regulate cytokine secretion in inflamed tissues.
