| First Author | Chen C | Year | 2006 |
| Journal | Immunity | Volume | 25 |
| Issue | 6 | Pages | 895-906 |
| PubMed ID | 17137800 | Mgi Jnum | J:116615 |
| Mgi Id | MGI:3694582 | Doi | 10.1016/j.immuni.2006.10.013 |
| Citation | Chen C, et al. (2006) The Integrin alpha9beta1 contributes to granulopoiesis by enhancing granulocyte colony-stimulating factor receptor signaling. Immunity 25(6):895-906 |
| abstractText | The integrin alpha9beta1 is widely expressed on neutrophils, smooth muscle, hepatocytes, endothelia, and some epithelia. We now show that mice lacking this integrin have a dramatic defect in neutrophil development, with decreased numbers of granulocyte precursors in bone marrow and impaired differentiation of bone marrow cells into granulocytes. In response to granulocyte colony-stimulating factor (G-CSF), alpha9-deficient bone marrow cells or human bone marrow cells incubated with alpha9beta1-blocking antibody demonstrated decreased phosphorylation of signal transducer and activator of transcription 3 and extracellular signal-regulated protein kinase. These effects depended on the alpha9 subunit cytoplasmic domain, which was required for formation of a physical complex between alpha9beta1 and ligated G-CSF receptor. Integrin alpha9beta1 was required for granulopoiesis and played a permissive role in the G-CSF-signaling pathway, suggesting that this integrin could play an important role in disorders of granulocyte development and other conditions characterized by defective G-CSF signaling. |
