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Opposite effects of Trichostatin A on activation of mast cells by different stimulants
Author(s) -
Wang Qing-hui,
Nishiyama Chiharu,
Nakano Nobuhiro,
Kanada Shunsuke,
Hara Mutsuko,
Kitamura Nao,
Shimokawa Naomi,
Lu Chang-long,
Ogawa Hideoki,
Okumura Ko
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.03.047
Subject(s) - trichostatin a , chromatin immunoprecipitation , chemistry , immunoglobulin e , stimulation , microbiology and biotechnology , transcription factor , chromatin , immunology , cancer research , histone deacetylase , biology , antibody , promoter , histone , endocrinology , biochemistry , gene expression , gene
Mast cells (MCs) are activated upon stimulation via TLRs or FcεRI, contributing to immune protection and/or leading to allergic diseases. In the present study, the effects of Trichostatin A (TSA) on the activation of MCs were analyzed with bone marrow‐derived (BM) MCs. TSA increased the transcription and protein secretion of IL‐6 in case of LPS‐stimulation, in contrast to the suppressive effect on IgE‐mediated activation of BMMCs. Chromatin immunoprecipitation assay showed IgE‐mediated signaling‐specific suppression of transcription factors recruitment to the IL‐6 promoter. TSA‐treatment inhibited nuclear translocation of NF‐κB following IgE‐mediated, but not LPS‐induced activation in MCs.