Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules

Haiyan Song; Nobuhiro Shojima; Hideyuki Sakoda; Takehide Ogihara; Midori Fujishiro; Hideki Katagiri; Motonobu Anai; Yukiko Onishi; Hiraku Ono; Kouichi Inukai; Yasushi Fukushima; Masatoshi Kikuchi; Hitoshi Shimano; Nobuhiro Yamada; Yoshitomo Oka; Tomoichiro Asano

doi:10.1016/S0006-291X(02)02551-2

Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules

Haiyan Song, Nobuhiro Shojima, Hideyuki Sakoda, Takehide Ogihara, Midori Fujishiro, Hideki Katagiri, Motonobu Anai, Yukiko Onishi, Hiraku Ono, Kouichi Inukai, Yasushi Fukushima, Masatoshi Kikuchi, Hitoshi Shimano, Nobuhiro Yamada, Yoshitomo Oka, Tomoichiro Asano

MED - Medical Sciences

The University of Tokyo

Research output: Contribution to journal › Article › peer-review

67 Citations (Scopus)

Abstract

Expression of the adipocyte-derived protein resistin, which is thought to play a key role in the development of insulin resistance in vivo, is regulated by a variety of hormones and mediators, including insulin and TNFα. Here we describe our use of adenovirus-mediated gene transfer to determine which transcription factors and signaling pathways affect resistin expression in 3T3-L1 adipocytes. We found that resistin expression was enhanced by overexpression of C/EBPα and suppressed by C/EBPζ, a negative regulator of C/EBPα. Additionally, C/EBPα induced resistin even in L6 myocytes. Overexpression of PPARγ markedly reduced resistin expressi on, whereas PPARα had no significant effect. Resistin expression was markedly suppressed by overexpression of the PI3-kinase p110α catalytic subunit and by Akt. Finally, overexpression of MEK1, MKK6, or MKK7 suppressed resistin expression. These findings indicate that resistin expression is regulated by C/EBPα and PPARγ, partly via modulation of signal transduction in the PI3-kinase and MAP kinase pathways.

Original language	English
Pages (from-to)	291-298
Number of pages	8
Journal	Biochemical and Biophysical Research Communications
Volume	299
Issue number	2
DOIs	https://doi.org/10.1016/S0006-291X(02)02551-2
Publication status	Published - 2002

Keywords

Adipocyte
Adipogenesis PPARs
C/EBPs
MAP kinase
PI3-kinase
Resistin
Signal transduction
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10.1016/S0006-291X(02)02551-2

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Song, H., Shojima, N., Sakoda, H., Ogihara, T., Fujishiro, M., Katagiri, H., Anai, M., Onishi, Y., Ono, H., Inukai, K., Fukushima, Y., Kikuchi, M., Shimano, H., Yamada, N., Oka, Y., & Asano, T. (2002). Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules. Biochemical and Biophysical Research Communications, 299(2), 291-298. https://doi.org/10.1016/S0006-291X(02)02551-2

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title = "Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules",

abstract = "Expression of the adipocyte-derived protein resistin, which is thought to play a key role in the development of insulin resistance in vivo, is regulated by a variety of hormones and mediators, including insulin and TNFα. Here we describe our use of adenovirus-mediated gene transfer to determine which transcription factors and signaling pathways affect resistin expression in 3T3-L1 adipocytes. We found that resistin expression was enhanced by overexpression of C/EBPα and suppressed by C/EBPζ, a negative regulator of C/EBPα. Additionally, C/EBPα induced resistin even in L6 myocytes. Overexpression of PPARγ markedly reduced resistin expressi on, whereas PPARα had no significant effect. Resistin expression was markedly suppressed by overexpression of the PI3-kinase p110α catalytic subunit and by Akt. Finally, overexpression of MEK1, MKK6, or MKK7 suppressed resistin expression. These findings indicate that resistin expression is regulated by C/EBPα and PPARγ, partly via modulation of signal transduction in the PI3-kinase and MAP kinase pathways.",

keywords = "Adipocyte, Adipogenesis PPARs, C/EBPs, MAP kinase, PI3-kinase, Resistin, Signal transduction, Transcription",

author = "Haiyan Song and Nobuhiro Shojima and Hideyuki Sakoda and Takehide Ogihara and Midori Fujishiro and Hideki Katagiri and Motonobu Anai and Yukiko Onishi and Hiraku Ono and Kouichi Inukai and Yasushi Fukushima and Masatoshi Kikuchi and Hitoshi Shimano and Nobuhiro Yamada and Yoshitomo Oka and Tomoichiro Asano",

year = "2002",

doi = "10.1016/S0006-291X(02)02551-2",

language = "English",

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journal = "Biochemical and Biophysical Research Communications",

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Song, H, Shojima, N, Sakoda, H, Ogihara, T, Fujishiro, M, Katagiri, H, Anai, M, Onishi, Y, Ono, H, Inukai, K, Fukushima, Y, Kikuchi, M, Shimano, H, Yamada, N, Oka, Y & Asano, T 2002, 'Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules', Biochemical and Biophysical Research Communications, vol. 299, no. 2, pp. 291-298. https://doi.org/10.1016/S0006-291X(02)02551-2

TY - JOUR

T1 - Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules

AU - Song, Haiyan

AU - Shojima, Nobuhiro

AU - Sakoda, Hideyuki

AU - Ogihara, Takehide

AU - Fujishiro, Midori

AU - Katagiri, Hideki

AU - Anai, Motonobu

AU - Onishi, Yukiko

AU - Ono, Hiraku

AU - Inukai, Kouichi

AU - Fukushima, Yasushi

AU - Kikuchi, Masatoshi

AU - Shimano, Hitoshi

AU - Yamada, Nobuhiro

AU - Oka, Yoshitomo

AU - Asano, Tomoichiro

PY - 2002

Y1 - 2002

N2 - Expression of the adipocyte-derived protein resistin, which is thought to play a key role in the development of insulin resistance in vivo, is regulated by a variety of hormones and mediators, including insulin and TNFα. Here we describe our use of adenovirus-mediated gene transfer to determine which transcription factors and signaling pathways affect resistin expression in 3T3-L1 adipocytes. We found that resistin expression was enhanced by overexpression of C/EBPα and suppressed by C/EBPζ, a negative regulator of C/EBPα. Additionally, C/EBPα induced resistin even in L6 myocytes. Overexpression of PPARγ markedly reduced resistin expressi on, whereas PPARα had no significant effect. Resistin expression was markedly suppressed by overexpression of the PI3-kinase p110α catalytic subunit and by Akt. Finally, overexpression of MEK1, MKK6, or MKK7 suppressed resistin expression. These findings indicate that resistin expression is regulated by C/EBPα and PPARγ, partly via modulation of signal transduction in the PI3-kinase and MAP kinase pathways.

AB - Expression of the adipocyte-derived protein resistin, which is thought to play a key role in the development of insulin resistance in vivo, is regulated by a variety of hormones and mediators, including insulin and TNFα. Here we describe our use of adenovirus-mediated gene transfer to determine which transcription factors and signaling pathways affect resistin expression in 3T3-L1 adipocytes. We found that resistin expression was enhanced by overexpression of C/EBPα and suppressed by C/EBPζ, a negative regulator of C/EBPα. Additionally, C/EBPα induced resistin even in L6 myocytes. Overexpression of PPARγ markedly reduced resistin expressi on, whereas PPARα had no significant effect. Resistin expression was markedly suppressed by overexpression of the PI3-kinase p110α catalytic subunit and by Akt. Finally, overexpression of MEK1, MKK6, or MKK7 suppressed resistin expression. These findings indicate that resistin expression is regulated by C/EBPα and PPARγ, partly via modulation of signal transduction in the PI3-kinase and MAP kinase pathways.

KW - Adipocyte

KW - Adipogenesis PPARs

KW - C/EBPs

KW - MAP kinase

KW - PI3-kinase

KW - Resistin

KW - Signal transduction

KW - Transcription

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U2 - 10.1016/S0006-291X(02)02551-2

DO - 10.1016/S0006-291X(02)02551-2

M3 - Article

C2 - 12437985

AN - SCOPUS:0036434112

SN - 0006-291X

VL - 299

SP - 291

EP - 298

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 2

ER -

Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules

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Keywords

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