Response gene to complement 32 protein promotes macrophage phagocytosis via activation of protein kinase C pathway.
Macrophage phagocytosis plays an important role in host defense. The molecular mechanism, especially factors regulating the phagocytosis, however, is not completely understood. In the present study, we found that response gene to complement 32 (RGC-32) is an important regulator of phagocytosis. Although RGC-32 is induced and abundantly expressed in macrophage during monocyte-macrophage differentiation, RGC-32 appears not to be important for this process because RGC-32-deficient bone marrow progenitor can normally differentiate to macrophage. However, both peritoneal macrophages and bone marrow-derived macrophages with RGC-32 deficiency exhibit significant defects in phagocytosis, whereas RGC-32-overexpressed macrophages show increased phagocytosis. Mechanistically, RGC-32 is recruited to macrophage membrane where it promotes F-actin assembly and the formation of phagocytic cups. RGC-32 knock-out impairs F-actin assembly. RGC-32 appears to interact with PKC to regulate PKC-induced phosphorylation of F-actin cross-linking protein myristoylated alanine-rich protein kinase C substrate. Taken together, our results demonstrate for the first time that RGC-32 is a novel membrane regulator for macrophage phagocytosis.
['Tang|Rui|R|', 'Zhang|Gui|G|', 'Chen|Shi-You|SY|']
D000199:Actins D000818:Animals D018797:Cell Cycle Proteins D045744:Cell Line, Tumor D002462:Cell Membrane D006801:Humans D017737:Macrophages, Peritoneal D051379:Mice D018345:Mice, Knockout D009124:Muscle Proteins D009419:Nerve Tissue Proteins D009687:Nuclear Proteins D010587:Phagocytosis D010766:Phosphorylation D011493:Protein Kinase C
Response Gene to Complement 32 Macrophage Phagocytosis Actin Protein Kinase C (PKC) Signal Transduction