A novel murine α4 integrin splicing variant is a specific receptor for VCAM-1 (61.2)

Abstract

Abstract Integrins affect multiple cell motility in control of cell survival, growth, or differentiation mediated by cell-cell and cell-extracellular matrix interaction. We previously reported that α9 integrin splicing variant, SFα9, promotes wild type α9 integrin-dependent adhesion. In this report, we introduce a new murine α4 integrin splicing variant mSFα4, which have new short cytoplasmic tail. In inflamed tissues including rheumatoid joint, the expression of mSFa4, as well as wild type α4 integrin, is upregulated. Interestingly, cells expressing mSFα4 bind to VCAM-1 but not other α4 integrin ligand such as fibronectin CS1 or osteopontin. Binding of cells coexpressing mSFα4 and wild type α4 integrin to α4 integrin ligands is promoted than cells expressing wild type α4 integrin. Thus, mSFα4 functions modulation of α4 integrin. Now, we pursue the metastatic function of mSFα4 by using mSFα4-specific knockdown tumor cells.