Distinct roles for the SgIGSF adhesion molecule and c-kit receptor tyrosine kinase in the interaction between mast cells and the mesentery.
Intraperitoneal injection of bone marrow-derived mast cells (BMMCs) has therapeutic efficacy against acute bacterial peritonitis. For this role, BMMCs need to settle down the mesentery from the peritoneal cavity. Interaction between BMMCs and the mesentery was examined by using mast cell deficient WBB6F1(F1)-W/Wv [c-kit receptor tyrosine kinase (KIT) mutant], F1-Sl/Sld [KIT ligand stem cell factor mutant], and F1-tg/tg [a practically microphthalmia transcription factor (MITF)-null mutant] mice. Three parameters were measured: the number of BMMCs: (1) developed in the mesentery 5 weeks after intraperitoneal injection into mast cell deficient mice, (2) adhered to mesenteric mesothelial cells, and (3) transmigrated across the mesenteric mesothelial cell monolayer when coculturing both cells for 3 and 18 h, respectively. After intraperitoneal injection, F1-wild type (+/+) BMMCs developed in the mesentery of F1-W/Wv mice but not in that of F1-Sl/Sld mice, while F1-tg/tg BMMCs did not develop, even in the mesentery of WBB6F1-W/Wv mice. In the coculture, WB-W/W BMMCs normally adhered to but poorly transmigrated across F1-+/+ mesothelial cells, and in accordance, F1-+/+ BMMCs normally adhered to but poorly transmigrated across F1-Sl/Sld mesothelial cells. F1-tg/tg BMMCs showed poor adhesion and transmigration, but both parameters were partially but significantly improved by ectopic expression of spermatogenic immunoglobulin superfamily (SgIGSF), a mast-cell adhesion molecule critically regulated by MITF. Since F1-tg/tg BMMCs expressed reduced levels of KIT, these results suggested that SgIGSF and KIT independently played a significant role in the transmigration. Among three parameters, development of mast cells in the mesentery well correlated with the transmigration. This process seemed important for mast cells to settle down from the peritoneal cavity to the mesentery.
Department of Pathology, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan.
Kenji
K
Watabe
Akihiko
A
Ito
Yu-Ichiro
Y
Koma
Tomohiko
T
Wakayama
Shoichi
S
Iseki
Yasuhisa
Y
Shinomura
Yukihiko
Y
Kitamura
D000818:Animals; D015153:Blotting, Western; D001854:Bone Marrow Cells / Q000166:cytology; D002448:Cell Adhesion; D000075982:Cell Adhesion Molecule-1; D015815:Cell Adhesion Molecules; D002465:Cell Movement; D002478:Cells, Cultured; D003433:Crosses, Genetic; D005434:Flow Cytometry; D005786:Gene Expression Regulation; D005822:Genetic Vectors; D007136:Immunoglobulins / Q000502:physiology*; D007150:Immunohistochemistry; D008407:Mast Cells / Q000166:cytology*; D008565:Membrane Proteins / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation; D041681:NIH 3T3 Cells; D011485:Protein Binding; D019009:Proto-Oncogene Proteins c-kit / Q000737:chemistry*; D012190:Retroviridae / Q000235:genetics; D013997:Time Factors; D014162:Transfection
C498598:Cadm1 protein, mouse; D000075982:Cell Adhesion Molecule-1; D015815:Cell Adhesion Molecules; D007136:Immunoglobulins; D008565:Membrane Proteins; D019009:Proto-Oncogene Proteins c-kit