Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions

Masayuki Funaba, Teruo Ikeda, Masaru Murakami, Kenji Ogawa, Yoshii Nishino, Kunihiro Tsuchida, Hiromu Sugino, Matanobu Abe

研究成果: ジャーナルへの寄稿学術論文査読

11 被引用数 (Scopus)

抄録

Transforming growth factor-β (TGF-β) 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-β-mediated cell responses in BMMCs. Treating BMMCs with TGF-β induced the phosphorylation of p38 within 2 h and persisted for 24 h. The involvement of p38 in TGF-β-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-β 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-β treatment was smaller in Smad3-deficient BMMCs compared to wild-type BMMCs. Maximal migration was detected at a TGF-β concentration of 40 fM in wild-type BMMCs, whereas TGF-β-induced migration was absent in Smad3-deficient BMMCs. Thus, the roles of p38 and Smad3 are different among TGF-β-mediated cell responses in BMMCs.

本文言語英語
ページ(範囲)2154-2161
ページ数8
ジャーナルCellular Signalling
18
12
DOI
出版ステータス出版済み - 12-2006
外部発表はい

All Science Journal Classification (ASJC) codes

  • 細胞生物学

フィンガープリント

「Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル