Regulation of the interleukin-3 (IL-3) receptor by IL-3 in the fetal
liver-derived FL5.12 cell line
PA Algate, LS Steelman, MW Mayo, A Miyajima and JA McCubrey
Department of Microbiology and Immunology, East Carolina University School
of Medicine, Greenville, NC 27858.
To determine the effects of a cytokine on cognate receptor expression in
normal and neoplastic cells, the interleukin-3 receptor (IL-3R) complex was
examined in the parental IL-3-dependent line FL5.12, which was isolated
from fetal liver, and in autocrine- and v-abl-transformed derivative lines.
IL-3 decreased the amount of the IL-3R alpha and beta chains detected on
the cell surface of the parental IL-3-dependent cells. In contrast, high
levels of IL-3R beta were constitutively detected on the
autocrine-transformed lines in the absence and presence of exogenous IL-3.
Only low levels of IL-3R beta were observed in the two v-abl-transformed
derivative cell lines examined, which no longer required IL-3 for growth.
The levels of the IL-3R alpha chain detected were similar in these
transformed cells and were not regulated by IL-3. These results were
substantiated further by RNA analysis, because IL-3 decreased the levels of
IL-3R transcripts in the parental factor- dependent FL5.12 line. The
pattern of IL-3R gene expression was opposite to that of other receptors or
proto-oncogenes, because RNA transcripts for all other genes examined were
induced by IL-3. We conclude that IL-3 tightly controls IL-3R expression in
the IL-3- dependent FL5.12 cells, whereas steady-state mRNA levels were not
altered in the two v-abl-transformed derivative cell lines examined in this
study.
Volume 83,
Issue 9,
pp. 2459-2468,
05/01/1994
Copyright © 1994 by The American Society of Hematology
