Molecular mechanisms of HGF-beta-induced macrophage phagocytosis

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We provide evidence that hepatocyte growth factor (HGF) beta-chain remnant (HGF-beta), generated through fragmentation of HGF by proteases released from inflammatory cells such as neutrophils, potently stimulated phagocytosis of apoptotic neutrophils by binding to mannose receptor (MR), which recently identified as an HGF-beta receptor. Upon binding to MR, HGF-beta may modulate actin cytoskeleton and enhance phagocytosis through interaction between MR and actin-binding protein IQGAP1. HGF-beta also induced surface expression of CD11b, a component of receptor complex required for complement-mediated phagocytosis. These findings suggest that HGF-beta/MR axis-induced macrophage phagocytosis could prevent accumulation of apoptotic neutrophils and release of inflammatory molecules from neutrophils, which leads to resolution of inflammation and promotion of tissue repair.