Involvement of P38 Map Kinase and Smad3 in Tgf-beta-mediated Mast Cell Functions.
From: Laboratory of Nutrition, Azabu University School of Veterinary Medicine, 1-17-71 Fuchinobe, Sagamihara 229-8501, Japan. funaba@azabu-u.ac.jp
Cellular signalling
- Publish Date: Dec 2006
- ISSN: 0898-6568
- Volume: 18
- Issue: 12
- Pages: 2154-61
- Medium: Print
- Language: English
- Citation (JAMA): Funaba Masayuki, Ikeda Teruo, Murakami Masaru, et al. Involvement of P38 Map Kinase and Smad3 in Tgf-beta-mediated Mast Cell Functions.. Cell. Signal. Dec 2006;18:2154-61
Abstract
Transforming growth factor-beta (TGF-beta) modulates functions of bone marrow-derived cultured mast cells (BMMCs); cell maturation (up-regulation of mouse mast cell proteases (mmcps)), growth arrest and migration. We investigated the roles of p38 MAP kinase and Smad3 in TGF-beta-mediated cell responses in BMMCs. Treating BMMCs with TGF-beta induced the phosphorylation of p38 within 2 h and persisted for 24 h. The involvement of p38 in TGF-beta-induced cell responses depended upon mast cell functions; it was necessary for up-regulation of mmcp-1 and migration, but not for up-regulation of mmcp-7 and inhibition of metabolic activity. New protein synthesis was required for the up-regulation of mmcp-1 but not mmcp-7 in response to TGF-beta treatment, and stabilization of mRNA was partially responsible for the increase in gene transcript of mmcp-1. The decrease in metabolic activity in response to TGF-beta treatment was smaller in Smad3-deficient BMMCs compared to wild-type BMMCs. Maximal migration was detected at a TGF-beta concentration of 40 fM in wild-type BMMCs, whereas TGF-beta-induced migration was absent in Smad3-deficient BMMCs. Thus, the roles of p38 and Smad3 are different among TGF-beta-mediated cell responses in BMMCs.
Mesh Headings (Keywords): Animals, Anthracenes, Blotting, Western, Bone Marrow Cells, Cell Movement, Cell Proliferation, Cells, Cultured, Chymases, Dose-Response Relationship, Drug, Enzyme Inhibitors, Flavonoids, Imidazoles, Mast Cells, Mice, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Knockout, Phosphorylation, Pyridines, RNA, Messenger, Reverse Transcriptase Polymerase Chain Reaction, Smad3 Protein, Transforming Growth Factor beta, Tryptases, Up-Regulation, p38 Mitogen-Activated Protein Kinases
Check for Full Text / PubMed Unique Identifier (PMID): 16750902
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