Krüppel-like transcription factor KLF5 is a key regulator of adipocyte differentiation

Yumiko Oishi; Ichiro Manabe; Kazuyuki Tobe; Kensuke Tsushima; Takayuki Shindo; Katsuhito Fujiu; Go Nishimura; Koji Maemura; Toshimasa Yamauchi; Naoto Kubota; Ryo Suzuki; Toshio Kitamura; Shizuo Akira; Takashi Kadowaki; Ryozo Nagai

doi:10.1016/j.cmet.2004.11.005

Krüppel-like transcription factor KLF5 is a key regulator of adipocyte differentiation

Yumiko Oishi, Ichiro Manabe, Kazuyuki Tobe, Kensuke Tsushima, Takayuki Shindo, Katsuhito Fujiu, Go Nishimura, Koji Maemura, Toshimasa Yamauchi, Naoto Kubota, Ryo Suzuki, Toshio Kitamura, Shizuo Akira, Takashi Kadowaki, Ryozo Nagai^*

^*Corresponding author for this work

Faculty of Medicine

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

386 Scopus citations

Abstract

Krüppel-like factor 5 (KLF5) is a zinc-finger transcription factor known to play a pivotal role in the pathogenesis of cardiovascular disease. Here, we show that neonatal heterozygous KLF5 knockout mice exhibit a marked deficiency in white adipose tissue development, suggesting that KLF5 is also required for adipogenesis. In 3T3-L1 preadipocytes, KLF5 expression was induced at an early stage of differentiation, and this was followed by expression of PPARγ₂. Constitutive overexpression of dominant-negative KLF5 inhibited adipocyte differentiation, whereas overexpression of wild-type KLF5 induced differentiation even without hormonal stimulation. Moreover, embryonic fibroblasts obtained from KLF5^+/- mice showed much attenuated adipocyte differentiation, confirming the key role played by KLF5 in adipocyte differentiation. KLF5 expression is induced by C/EBPβ and δ. KLF5, in turn, acts in concert with C/EBPβ/δ to activate the PPARγ₂ promoter. This study establishes KLF5 as a key component of the transcription factor network controlling adipocyte differentiation.

Original language	English
Pages (from-to)	27-39
Number of pages	13
Journal	Cell Metabolism
Volume	1
Issue number	1
DOIs	https://doi.org/10.1016/j.cmet.2004.11.005
State	Published - 2005/01

ASJC Scopus subject areas

Physiology
Molecular Biology
Cell Biology

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10.1016/j.cmet.2004.11.005

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@article{a9a5285604d849449bcc107a7acb1c65,

title = "Kr{\"u}ppel-like transcription factor KLF5 is a key regulator of adipocyte differentiation",

abstract = "Kr{\"u}ppel-like factor 5 (KLF5) is a zinc-finger transcription factor known to play a pivotal role in the pathogenesis of cardiovascular disease. Here, we show that neonatal heterozygous KLF5 knockout mice exhibit a marked deficiency in white adipose tissue development, suggesting that KLF5 is also required for adipogenesis. In 3T3-L1 preadipocytes, KLF5 expression was induced at an early stage of differentiation, and this was followed by expression of PPARγ2. Constitutive overexpression of dominant-negative KLF5 inhibited adipocyte differentiation, whereas overexpression of wild-type KLF5 induced differentiation even without hormonal stimulation. Moreover, embryonic fibroblasts obtained from KLF5+/- mice showed much attenuated adipocyte differentiation, confirming the key role played by KLF5 in adipocyte differentiation. KLF5 expression is induced by C/EBPβ and δ. KLF5, in turn, acts in concert with C/EBPβ/δ to activate the PPARγ2 promoter. This study establishes KLF5 as a key component of the transcription factor network controlling adipocyte differentiation.",

author = "Yumiko Oishi and Ichiro Manabe and Kazuyuki Tobe and Kensuke Tsushima and Takayuki Shindo and Katsuhito Fujiu and Go Nishimura and Koji Maemura and Toshimasa Yamauchi and Naoto Kubota and Ryo Suzuki and Toshio Kitamura and Shizuo Akira and Takashi Kadowaki and Ryozo Nagai",

note = "Funding Information: We gratefully acknowledge Eriko Magoshi and Noriko Yamanaka for their excellent technical assistance. This study was supported in part by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science and Technology, Japan (to R.N. and I.M.), and research grants from Mitsubishi Pharma Research Foundation and Kanae Foundation for Life & Socio-Medical Science (to I.M.). ",

year = "2005",

month = jan,

doi = "10.1016/j.cmet.2004.11.005",

language = "英語",

volume = "1",

pages = "27--39",

journal = "Cell Metabolism",

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publisher = "Cell Press",

number = "1",

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TY - JOUR

T1 - Krüppel-like transcription factor KLF5 is a key regulator of adipocyte differentiation

AU - Oishi, Yumiko

AU - Manabe, Ichiro

AU - Tobe, Kazuyuki

AU - Tsushima, Kensuke

AU - Shindo, Takayuki

AU - Fujiu, Katsuhito

AU - Nishimura, Go

AU - Maemura, Koji

AU - Yamauchi, Toshimasa

AU - Kubota, Naoto

AU - Suzuki, Ryo

AU - Kitamura, Toshio

AU - Akira, Shizuo

AU - Kadowaki, Takashi

AU - Nagai, Ryozo

N1 - Funding Information: We gratefully acknowledge Eriko Magoshi and Noriko Yamanaka for their excellent technical assistance. This study was supported in part by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science and Technology, Japan (to R.N. and I.M.), and research grants from Mitsubishi Pharma Research Foundation and Kanae Foundation for Life & Socio-Medical Science (to I.M.).

PY - 2005/1

Y1 - 2005/1

N2 - Krüppel-like factor 5 (KLF5) is a zinc-finger transcription factor known to play a pivotal role in the pathogenesis of cardiovascular disease. Here, we show that neonatal heterozygous KLF5 knockout mice exhibit a marked deficiency in white adipose tissue development, suggesting that KLF5 is also required for adipogenesis. In 3T3-L1 preadipocytes, KLF5 expression was induced at an early stage of differentiation, and this was followed by expression of PPARγ2. Constitutive overexpression of dominant-negative KLF5 inhibited adipocyte differentiation, whereas overexpression of wild-type KLF5 induced differentiation even without hormonal stimulation. Moreover, embryonic fibroblasts obtained from KLF5+/- mice showed much attenuated adipocyte differentiation, confirming the key role played by KLF5 in adipocyte differentiation. KLF5 expression is induced by C/EBPβ and δ. KLF5, in turn, acts in concert with C/EBPβ/δ to activate the PPARγ2 promoter. This study establishes KLF5 as a key component of the transcription factor network controlling adipocyte differentiation.

AB - Krüppel-like factor 5 (KLF5) is a zinc-finger transcription factor known to play a pivotal role in the pathogenesis of cardiovascular disease. Here, we show that neonatal heterozygous KLF5 knockout mice exhibit a marked deficiency in white adipose tissue development, suggesting that KLF5 is also required for adipogenesis. In 3T3-L1 preadipocytes, KLF5 expression was induced at an early stage of differentiation, and this was followed by expression of PPARγ2. Constitutive overexpression of dominant-negative KLF5 inhibited adipocyte differentiation, whereas overexpression of wild-type KLF5 induced differentiation even without hormonal stimulation. Moreover, embryonic fibroblasts obtained from KLF5+/- mice showed much attenuated adipocyte differentiation, confirming the key role played by KLF5 in adipocyte differentiation. KLF5 expression is induced by C/EBPβ and δ. KLF5, in turn, acts in concert with C/EBPβ/δ to activate the PPARγ2 promoter. This study establishes KLF5 as a key component of the transcription factor network controlling adipocyte differentiation.

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JO - Cell Metabolism

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ER -

Krüppel-like transcription factor KLF5 is a key regulator of adipocyte differentiation

Abstract

ASJC Scopus subject areas

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