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MIP-3alpha Induces Human Eosinophil Migration and Activation of the Mitogen-Activated Protein Kinases (p42/p44 MAPK)

S K Sullivan, D A McGrath, F Liao, S A Boehme, J M Farber, K B Bacon

J Leukoc Biol. 1999 Oct;66(4):674-82.

PMID: 10534125

Abstract:

The CC chemokine macrophage inflammatory protein-3alpha (MIP-3alpha) is the product of recent electronic cloning efforts, however, little characterization of its spectrum of biological effects has been undertaken. Human eosinophils exhibited pertussis-toxin-sensitive migration in response to human recombinant (hr)MIP-3alpha. Messenger RNA for the MIP-3alpha receptor, CCR-6, and low levels of surface expression were demonstrated by reverse transcriptase-polymerase chain reaction and FACS analysis. Analyses of cell signaling revealed dose-dependent increases in intracellular calcium mobilization, calcium transients that were, however, greatly reduced when compared with MCP-3-induced responses. Further investigations of MIP-3alpha-induced signal transduction revealed time- and dose-dependent, partially pertussis toxin-dependent, increases in phosphorylation of the p42/p44 mitogen-activated protein kinases (MAPK) that occurred at 10- to 100-fold lower concentrations, and that were linked to a phosphoinositide 3-kinase pathway. These results suggest that MIP-3alpha can regulate multiple, parallel signal transduction pathways in eosinophils, and suggest that MAPK activation by MIP-3alpha in eosinophils is a significant signaling pathway for migration induction.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
IAR42413126 MIP-3alpha human MIP-3alpha human Price
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