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Mechanism of mast cell deficiency in mutant mice of mi/mi genotype: an
analysis by co-culture of mast cells and fibroblasts
Y Ebi, T Kasugai, Y Seino, H Onoue, T Kanemoto and Y Kitamura
Department of Pathology, Osaka University Medical School, Japan.
Mutant mice of mi/mi genotype are osteopetrotic and are deficient in mast
cells. The osteopetrosis of mi/mi mice can be cured by bone marrow
transplantation from congenic normal (+/+) mice, and therefore, the cause
of the osteopetrosis is attributed to a defect of osteoclasts. Since both
osteoclasts and mast cells are the progeny of multipotential hematopoietic
stem cells, we examined whether mast cells were defective in mi/mi mice. In
spite of the deficiency of mast cells in tissues of mi/mi mice, mast cells
did develop when spleen cells of mi/mi mice were cultured with pokeweed
mitogen-stimulated spleen cell conditioned medium (PWM-SCM). The
proliferative response of cultured mast cells (CMC) derived from mi/mi mice
to PWM-SCM was comparable with that of CMC from +/+ mice. In contrast, when
CMC were co-cultured with the NIH/3T3 fibroblast cell line in culture
medium lacking PWM-SCM, only +/+ CMC entered into the S phase of the cell
cycle and were maintained; mi/mi CMC gradually disappeared. Moreover,
fibroblasts derived from the skin of mi/mi mice normally supported the
proliferation of +/+ CMC. Thus, the mast cell deficiency of mi/mi mice
appears to be due to the inability of mi/mi mast cells to respond to the
proliferative stimulus presented by fibroblasts.
Volume 75,
Issue 6,
pp. 1247-1251,
03/15/1990
Copyright © 1990 by The American Society of Hematology
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