| First Author | Zhang B | Year | 2009 |
| Journal | Eur J Immunol | Volume | 39 |
| Issue | 3 | Pages | 894-901 |
| PubMed ID | 19197940 | Mgi Jnum | J:146476 |
| Mgi Id | MGI:3837617 | Doi | 10.1002/eji.200838809 |
| Citation | Zhang B, et al. (2009) Akt2 is required for macrophage chemotaxis. Eur J Immunol 39(3):894-901 |
| abstractText | Tumor-associated macrophages play an important role in tumorigenesis and metastasis. Trafficking of macrophages to the proximity of tumors is mediated by CSF-1, a growth factor. In this study, we investigated the role of PKB/Akt in CSF-1-induced macrophage migration. Disruption of Akt2 expression by small interference RNA impaired chemotaxis of both THP-1 cells and mouse peritoneal macrophages. Phosphorylation of PKCzeta, an essential component in chemotaxis signaling pathway, was reduced. LIMK/Cofilin, downstream of PKCzeta, regulated cytoskeleton rearrangement during cell migration. Disruption of Akt2 expression inhibited CSF-1-induced LIMK/Cofilin phosphorylation, which contributed to defects in actin polymerization and chemotaxis. Furthermore, MCP-1, a chemokine, -induced macrophage chemotaxis was also impaired. Taken together, our results demonstrated that Akt2 plays an essential role in both CSF-1- and chemokine-induced chemotaxis of macrophages. |
