Interferon regulatory factor-2 is a transcriptional activator in muscle where it regulates expression of vascular cell adhesion molecule-1

被引:123
作者
Jesse, TL
LaChance, R
Iademarco, MF
Dean, DC
机构
[1] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Dept Cell Biol, St Louis, MO 63110 USA
关键词
D O I
10.1083/jcb.140.5.1265
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Previously, we have suggested that vascular cell adhesion molecule-1 (VCAM-1) and its integrin receptor alpha 4 beta 1 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 4 beta 1(+) 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.
引用
收藏
页码:1265 / 1276
页数:12
相关论文
共 45 条
[21]  
NEISH AS, 1995, MOL CELL BIOL, V15, P2558
[22]   INTERFERON CONSENSUS SEQUENCE-BINDING PROTEIN, A MEMBER OF THE INTERFERON REGULATORY FACTOR FAMILY, SUPPRESSES INTERFERON-INDUCED GENE-TRANSCRIPTION [J].
NELSON, N ;
MARKS, MS ;
DRIGGERS, PH ;
OZATO, K .
MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (01) :588-599
[23]  
NGUYEN H, 1995, ONCOGENE, V11, P537
[24]   CYTOARCHITECTURE OF THE FETAL MURINE SOLEUS MUSCLE [J].
ONTELL, M ;
BOURKE, D ;
HUGHES, D .
AMERICAN JOURNAL OF ANATOMY, 1988, 181 (03) :267-278
[25]   NEONATAL MUSCLE - ELECTRON-MICROSCOPIC STUDY [J].
ONTELL, M .
ANATOMICAL RECORD, 1977, 189 (04) :669-689
[26]   DIRECT EXPRESSION CLONING OF VASCULAR CELL-ADHESION MOLECULE-1, A CYTOKINE-INDUCED ENDOTHELIAL PROTEIN THAT BINDS TO LYMPHOCYTES [J].
OSBORN, L ;
HESSION, C ;
TIZARD, R ;
VASSALLO, C ;
LUHOWSKYJ, S ;
CHIROSSO, G ;
LOBB, R .
CELL, 1989, 59 (06) :1203-1211
[27]   Studies of Plasmodium falciparum cytoadherence using immortalized human brain capillary endothelial cells [J].
Prudhomme, JG ;
Sherman, IW ;
Land, KM ;
Moses, AV ;
Stenglein, S ;
Nelson, JA .
INTERNATIONAL JOURNAL FOR PARASITOLOGY, 1996, 26 (06) :647-655
[28]   CRITICAL ROLE OF A COMMON TRANSCRIPTION FACTOR, IRF-1, IN THE REGULATION OF IFN-BETA AND IFN-INDUCIBLE GENES [J].
REIS, LFL ;
HARADA, H ;
WOLCHOK, JD ;
TANIGUCHI, T ;
VILCEK, J .
EMBO JOURNAL, 1992, 11 (01) :185-193
[29]  
RICE GE, 1991, AM J PATHOL, V138, P385
[30]   ROLES FOR THE INTEGRIN VLA-4 AND ITS COUNTER RECEPTOR VCAM-1 IN MYOGENESIS [J].
ROSEN, GD ;
SANES, JR ;
LACHANCE, R ;
CUNNINGHAM, JM ;
ROMAN, J ;
DEAN, DC .
CELL, 1992, 69 (07) :1107-1119