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(American Journal of Pathology. 2004;165:491-499.)
© 2004 American Society for Investigative Pathology

Number of Mast Cells in the Peritoneal Cavity of Mice

Influence of Microphthalmia Transcription Factor through Transcription of Newly Found Mast Cell Adhesion Molecule, Spermatogenic Immunoglobulin Superfamily

Eiichi Morii^*, Akihiko Ito^*, Tomoko Jippo^*, Yu-ichiro Koma^*, Keisuke Oboki^*, Tomohiko Wakayama, Shoichi Iseki, M. Lynn Lamoreux and Yukihiko Kitamura^*

From the Department of Pathology,^* Medical School/Graduate School of Frontier Bioscience, Osaka University, Osaka, Japan; and the Department of Histology and Embryology, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan; and Laboratory Animal Resources and Research, Texas A & M University, College Station, Texas

The mi (microphthalmia) locus of mice encodes a transcription factor, MITF. B6-tg/tg mice that do not express any MITF have white coats and small eyes. Moreover, the number of mast cells decreased to one-third that of normal control (+/+) mice in the skin of B6-tg/tg mice. No mast cells were detectable in the stomach, mesentery, and peritoneal cavity of B6-tg/tg mice. Cultured mast cells derived from B6-tg/tg mice do not express a mast cell adhesion molecule, spermatogenic immunoglobulin superfamily (SgIGSF). To obtain in vivo evidence for the correlation of nonexpression of SgIGSF with decrease in mast cell number, we used another MITF mutant, B6-mi^vit/mi^vit mice that have a mild phenotype, ie, black coat with white patches and eyes of normal size. B6-mi^vit/mi^vit mice had a normal number of mast cells in the skin, stomach, and mesentery, but the number of peritoneal mast cells decreased to one-sixth that of +/+ mice. Cultured mast cells and peritoneal mast cells of B6-mi^vit/mi^vit mice showed a reduced but apparently detectable level of SgIGSF expression, demonstrating the parallelism between mast cell number and expression level of SgIGSF. The number of peritoneal mast cells appeared to be influenced by MITF through transcription of SgIGSF.