Abstract:
: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.
journal_name
Immunityjournal_title
Immunityauthors
Chen C,Huang X,Atakilit A,Zhu QS,Corey SJ,Sheppard Ddoi
10.1016/j.immuni.2006.10.013subject
Has Abstractpub_date
2006-12-01 00:00:00pages
895-906issue
6eissn
1074-7613issn
1097-4180pii
S1074-7613(06)00510-3journal_volume
25pub_type
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