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© The Rockefeller University Press, 0021-9525/1998//1265 $5.00
The Journal of Cell Biology, Volume 140, Number 5, , 1998 1265-1276

Article

Interferon Regulatory Factor-2 Is a Transcriptional Activator in Muscle Where It Regulates Expression of Vascular Cell Adhesion Molecule-1



Traci L. Jesse, Rhonda LaChance, Michael F. Iademarco, and Douglas C. Dean

Department of Medicine and Department of Cell Biology, Washington University School of Medicine, St. Louis, Missouri 63110

Previously, we have suggested that vascular cell adhesion molecule-1 (VCAM-1) and its integrin receptor {alpha}4β1 mediate cell–cell interactions important for skeletal myogenesis. Expression of the receptors subsequently subsides in muscle after birth. Here, we examine the mechanism regulating VCAM-1 gene expression in muscle. An enhancer located between the TATA box and the transcriptional start site is responsible for VCAM-1 gene expression in muscle—this element is inactive in endothelial cells where VCAM-1 expression is dependent on nuclear factor {kappa}B sites and inflammatory cytokines. We identify interferon regulatory factor-2 (IRF-2), a member of the interferon regulatory factor family, as the enhancer-binding transcription factor and show that expression of IRF-2 parallels that of VCAM-1 during mouse skeletal myogenesis. IRF-2 is not dependent upon cytokines for expression or activity, and it has been shown to act as a repressor in other nonmuscle cell types. We show that the basic repressor motif located near the COOH-terminal of IRF-2 is not active in muscle cells, but instead an acidic region in the center of the molecule functions as a transactivating domain. Although IRF-2 and VCAM-1 expression diminishes on adult muscle fiber, they are retained on myogenic stem cells (satellite cells). These satellite cells proliferate and fuse to regenerate muscle fiber after injury or disease. We present evidence that VCAM-1 on satellite cells mediates their interaction with {alpha}4β1(+) leukocytes that invade the muscle after injury or disease. We propose that VCAM-1 on endothelium generally recruits leukocytes to muscle after injury, whereas subsequent interaction with VCAM-1 on regenerating muscle cells focuses the invading leukocytes specifically to the sites of regeneration.

Abbreviations used in this paper: CAT, chloramphenicol acetyl transferase gene; E, embryonic day; IFN, interferon; IRF, interferon regulatory factor; VCAM-1, vascular cell adhesion molecule-1.


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