期刊
CELL CALCIUM
卷 45, 期 3, 页码 226-232出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2008.10.005
关键词
TRP channel; TRPM4; Mast cells; Actin cytoskeleton; Antigen; Migration; Transgenic mice
类别
资金
- Interuniversity Attraction Poles Programme Belgian State - Belgian Science Policy [P6/28]
- Flemish Government [EF/95/010]
- Uehara memorial foundation
- Deutsche Forschingsgemeinschaft
- Forschungsausschuss Universitat des Saarlandes
- HOMFOR program
We demonstrate here that the transient receptor potential melastatin subfamily channel, TRPM4, controls migration of bone marrow-derived mast cells (BMMCs), triggered by dinitrophenylated human serum albumin (DNP-HSA) or stem cell factor (SCF). Wild-type BMMCs migrate after stimulation with DNP-HSA or SCIF whereas both stimuli do not induce migration in BMMCs derived from TRPM4 knockout mice (trpm4(-/-)). Mast cell migration is a Ca2+-dependent process, and TRPM4 likely controls this process by setting the intracellular Ca2+ level upon cell stimulation. Cell migration depends on filamentous actin (F-actin) rearrangement, since pretreatment with cytochalasin B, an inhibitor of F-actin formation, prevented both DNP-HSA- and SCIF-incluced migration in wild-type BMMC. Immunocytochemical experiments using fluorescence-conjugated phalloidin demonstrate a reduced level of F-actin formation in DNP-HSA-stimulated BMMCs from trpm4(-/-) mice. Thus, our results suggest that TRPM4 is critically involved in migration of BMMCs by regulation of Ca2+-dependent actin cytoskeleton rearrangements. (c) 2008 Elsevier Ltd. All rights reserved.
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