Abstract
Intestinal epithelial cells have a remarkable capacity to migrate and efficiently reseal mucosal wounds that are characteristic of intestinal inflammatory diseases. In a recent study we reported that N-formyl peptide receptor-1 (FPR-1) is expressed in the intestinal epithelium and functions to regulate cell motility and wound closure. However, the mechanisms of FPR-1 induced epithelial cell migration are incompletely understood. Model intestinal epithelial cell lines were used to explore the signaling pathways by which FPR-1 activation promotes cell migration. Exposure of epithelial cells to the FPR-1 agonists, N-formyl methionyl peptide (fMLF) and Annexin 1 N-terminal peptide Ac2-26, induced rapid activation of PI3K. This correlated with guanine nucleotide exchange factor, Vav2 association with active Rac1 GTPase and its down-stream effector protein, Pak1. These events culminated in reactive oxygen species (ROS) generation and phosphorylation/activation of focal adhesion kinase (FAK) that in turn regulates cell migration. Taken together, these results support an important role for FPR-1 stimulated signaling pathways in promoting intestinal epithelial cell migration and wound closure.
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