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: Article

10 引用 (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.

元の言語English
ページ(範囲)2154-2161
ページ数8
ジャーナルCellular Signalling
18
発行部数12
DOI
出版物ステータスPublished - 01-12-2006

Fingerprint

Transforming Growth Factors
p38 Mitogen-Activated Protein Kinases
Mast Cells
Cultured Cells
Bone Marrow
Up-Regulation
Peptide Hydrolases
Phosphorylation
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Cell Biology

これを引用

Funaba, M., Ikeda, T., Murakami, M., Ogawa, K., Nishino, Y., Tsuchida, K., ... Abe, M. (2006). Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions. Cellular Signalling, 18(12), 2154-2161. https://doi.org/10.1016/j.cellsig.2006.04.005
Funaba, Masayuki ; Ikeda, Teruo ; Murakami, Masaru ; Ogawa, Kenji ; Nishino, Yoshii ; Tsuchida, Kunihiro ; Sugino, Hiromu ; Abe, Matanobu. / Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions. :: Cellular Signalling. 2006 ; 巻 18, 番号 12. pp. 2154-2161.
@article{0737bb6e3329406fb1063546186be51f,
title = "Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions",
abstract = "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.",
author = "Masayuki Funaba and Teruo Ikeda and Masaru Murakami and Kenji Ogawa and Yoshii Nishino and Kunihiro Tsuchida and Hiromu Sugino and Matanobu Abe",
year = "2006",
month = "12",
day = "1",
doi = "10.1016/j.cellsig.2006.04.005",
language = "English",
volume = "18",
pages = "2154--2161",
journal = "Cellular Signalling",
issn = "0898-6568",
publisher = "Elsevier Inc.",
number = "12",

}

Funaba, M, Ikeda, T, Murakami, M, Ogawa, K, Nishino, Y, Tsuchida, K, Sugino, H & Abe, M 2006, 'Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions', Cellular Signalling, 巻. 18, 番号 12, pp. 2154-2161. https://doi.org/10.1016/j.cellsig.2006.04.005

Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions. / Funaba, Masayuki; Ikeda, Teruo; Murakami, Masaru; Ogawa, Kenji; Nishino, Yoshii; Tsuchida, Kunihiro; Sugino, Hiromu; Abe, Matanobu.

:: Cellular Signalling, 巻 18, 番号 12, 01.12.2006, p. 2154-2161.

研究成果: Article

TY - JOUR

T1 - Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions

AU - Funaba, Masayuki

AU - Ikeda, Teruo

AU - Murakami, Masaru

AU - Ogawa, Kenji

AU - Nishino, Yoshii

AU - Tsuchida, Kunihiro

AU - Sugino, Hiromu

AU - Abe, Matanobu

PY - 2006/12/1

Y1 - 2006/12/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=33750356211&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33750356211&partnerID=8YFLogxK

U2 - 10.1016/j.cellsig.2006.04.005

DO - 10.1016/j.cellsig.2006.04.005

M3 - Article

C2 - 16750902

AN - SCOPUS:33750356211

VL - 18

SP - 2154

EP - 2161

JO - Cellular Signalling

JF - Cellular Signalling

SN - 0898-6568

IS - 12

ER -