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Poor response of cultured mast cells derived from mi/mi mutant mice to
nerve growth factor
T Jippo, H Ushio, S Hirota, H Mizuno, A Yamatodani, S Nomura, H Matsuda and Y Kitamura
Department of Pathology, Osaka University Medical School, Japan.
Decreased numbers of mast cells and abnormalities in the phenotype of mast
cells are observed in the skin of mi/mi mutant mice. Recently, the mi locus
was identified to encode a novel member of the basic-helix-
loop-helix-leucine zipper protein family of transcription factors. Since
nerve growth factor (NGF) has been reported to influence the proliferation
and the phenotype of cultured mast cells (CMCs), we compared the effect of
NGF between mi/mi and control normal (+/+) CMCs. Addition of NGF to the
suboptimal dose of recombinant murine interleukin-3 (rmIL-3) increased the
plating efficiency of +/+ CMCs, but not of mi/mi CMCs. Although +/+ CMCs
were berberine sulfate- negative when cultured with rmIL-3 alone, +/+ CMCs
became berberine sulfate-positive when cultured in the presence of both
rmIL-3 and NGF, which suggests increased heparin content. In contrast, NGF
did not influence the phenotype of mi/mi CMCs. +/+ CMCs significantly bound
125I-NGF, but mi/mi CMCs did not, which suggests a defect of NGF receptors
in mi/mi CMCs. Both p75 and p140 molecules are known to be involved in the
formation of NGF receptors. Although the expression of p140 messenger
(m)RNA was comparable between +/+ and mi/mi CMCs, the expression of p75
mRNA was significantly lower in mi/mi CMCs than in +/+ CMCs. Taken
together, the poor response of mi/mi CMCs to NGF appeared to be
attributable to the impaired transcription of the p75 gene.
Volume 84,
Issue 9,
pp. 2977-2983,
11/01/1994
Copyright © 1994 by The American Society of Hematology
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