title: Lipid raft-associated catechin suppresses the FcepsilonRI expression by inhibiting phosphorylation of the extracellular signal-regulated kinase1/2.
abstract: The major green tea catechin, (-)-epigallocatechin-3-O-gallate (EGCG), has a suppressive effect on the expression of the high-affinity IgE receptor FcepsilonRI, which is key molecule in the IgE-mediated allergic reactions. Here we show that EGCG binds to the cell surface and highly associates with plasma membrane microdomains, lipid rafts, on the human basophilic KU812 cells. The disruption of these lipid rafts caused a reduction of the amount of raft-associated EGCG and the FcepsilonRI-suppressive effect of EGCG. We also found that EGCG has an ability to inhibit the phosphorylation of the extracellular signal-regulated kinase1/2 (ERK1/2) and that the ERK1/2 specific inhibitor also reduced FcepsilonRI expression. Moreover, the inhibitory effect elicited by EGCG on ERK1/2 was prevented by disruption of rafts. Thus, these results suggest that the interaction between EGCG and the lipid rafts is important for EGCG's ability to downregulate FcepsilonRI expression, and ERK1/2 may be involved in this suppression signal.
authors.affiliation: Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, 812-8581, Fukuoka, Japan.
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Fujimura
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Tachibana
authors.forename: Koji
authors.initials: K
authors.lastname: Yamada
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis* / Q000737:chemistry; D001491:Basophils / Q000187:drug effects / Q000378:metabolism; D002392:Catechin / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000494:pharmacology*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D002784:Cholesterol / Q000378:metabolism / Q000494:pharmacology; D003505:Cyclodextrins / Q000494:pharmacology; D015536:Down-Regulation; D004791:Enzyme Inhibitors / Q000378:metabolism / Q000494:pharmacology; D005434:Flow Cytometry; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D015151:Immunoblotting; D021962:Membrane Microdomains / Q000378:metabolism*; D008565:Membrane Proteins; D019950:Mitogen-Activated Protein Kinase 1 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D010766:Phosphorylation; D017455:Receptors, IgE / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000737:chemistry; D047392:beta-Cyclodextrins
chemical_list: D015703:Antigens, CD; D003505:Cyclodextrins; D004791:Enzyme Inhibitors; C438731:MS4A7 protein, human; D008565:Membrane Proteins; D017455:Receptors, IgE; D047392:beta-Cyclodextrins; C108732:methyl-beta-cyclodextrin; D002392:Catechin; D002784:Cholesterol; C045651:epigallocatechin gallate; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases