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Arch. Immunol. Ther. Exp. (Warsz.) · Mar 2006
ReviewP-selectin mediates adhesion of leukocytes, platelets, and cancer cells in inflammation, thrombosis, and cancer growth and metastasis.
- Ming Chen and Jian-Guo Geng.
- Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Graduate School of Chinese Academy of Sciences, Shanghai, 200031, China.
- Arch. Immunol. Ther. Exp. (Warsz.). 2006 Mar 1; 54 (2): 75-84.
AbstractStimulated endothelial cells and activated platelets express P-selectin (CD62P), a member of the selectin family of cell adhesion molecules, which interacts with P-selectin glycoprotein ligand-1 (PSGL-1, CD162) for leukocyte rolling on stimulated endothelial cells and heterotypic aggregation of activated platelets onto leukocytes. Cross-linking of PSGL-1 by P-selectin also primes leukocytes intracellularly for cytokine and chemoattractant-induced beta2-integrin activation for firm adhesion of leukocytes. Furthermore, P-selectin mediates heterotypic aggregation of activated platelets to cancer cells and adhesion of cancer cells to stimulated endothelial cells. Here we provide a comprehensive summary of the functional roles and the biological importance of P-selectin-mediated cell adhesive interactions in the pathogeneses of inflammation, thrombosis, and the growth and metastasis of cancers.
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