A FoxO1-dependent, but NRF2-independent induction of heme oxygenase-1 during muscle atrophy

Jione Kang; Mi Gyeong Jeong; Sera Oh; Eun Jung Jang; Hyo Kyeong Kim; Eun Sook Hwang

doi:10.1016/j.febslet.2013.11.009

A FoxO1-dependent, but NRF2-independent induction of heme oxygenase-1 during muscle atrophy

Jione Kang, Mi Gyeong Jeong, Sera Oh, Eun Jung Jang, Hyo Kyeong Kim, Eun Sook Hwang

Pharmaceutical Sciences

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

41 Scopus citations

Abstract

Skeletal muscle plays key roles in metabolic homeostasis. Loss of muscle mass, called muscle atrophy exacerbates disease-associated metabolic perturbations. In this study, we characterized the molecular functions and mechanisms underlying regulation of skeletal muscle atrophy induced by denervation. Denervation significantly increased the expression of heme oxygenase-1 (HO-1) and atrogenes in skeletal muscle. Forkhead box protein O1 (FoxO1) drastically increased in atrophied muscle and selectively stimulated HO-1 gene transcription through direct DNA binding. Lack of HO-1 substantially attenuated muscle atrophy, whereas HO-1 overexpression caused muscle damage in vitro and in vivo. Collectively, HO-1 induced by FoxO1 may cause skeletal muscle atrophy.

Original language	English
Pages (from-to)	79-85
Number of pages	7
Journal	FEBS Letters
Volume	588
Issue number	1
DOIs	https://doi.org/10.1016/j.febslet.2013.11.009
State	Published - 3 Jan 2014

Keywords

FoxO1
MAFbx
MuRF1
NRF2
Nerve injury

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title = "A FoxO1-dependent, but NRF2-independent induction of heme oxygenase-1 during muscle atrophy",

abstract = "Skeletal muscle plays key roles in metabolic homeostasis. Loss of muscle mass, called muscle atrophy exacerbates disease-associated metabolic perturbations. In this study, we characterized the molecular functions and mechanisms underlying regulation of skeletal muscle atrophy induced by denervation. Denervation significantly increased the expression of heme oxygenase-1 (HO-1) and atrogenes in skeletal muscle. Forkhead box protein O1 (FoxO1) drastically increased in atrophied muscle and selectively stimulated HO-1 gene transcription through direct DNA binding. Lack of HO-1 substantially attenuated muscle atrophy, whereas HO-1 overexpression caused muscle damage in vitro and in vivo. Collectively, HO-1 induced by FoxO1 may cause skeletal muscle atrophy.",

keywords = "FoxO1, MAFbx, MuRF1, NRF2, Nerve injury",

author = "Jione Kang and Jeong, {Mi Gyeong} and Sera Oh and Jang, {Eun Jung} and Kim, {Hyo Kyeong} and Hwang, {Eun Sook}",

note = "Funding Information: We thank Dr. J. Alam (Alton Ochsner Medical Foundation, New Orleans) for providing pHO4.3k-luc vector and Ms. Hyun Jung Kim for helping histological analysis. This work was supported by the Basic research program ( 2012R1A1B3000603 for ESH and 2011-007983 for JOK) of the National Research Foundation funded by Ministry of Education, Science, and Technology.",

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doi = "10.1016/j.febslet.2013.11.009",

language = "English",

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T1 - A FoxO1-dependent, but NRF2-independent induction of heme oxygenase-1 during muscle atrophy

AU - Kang, Jione

AU - Jeong, Mi Gyeong

AU - Oh, Sera

AU - Jang, Eun Jung

AU - Kim, Hyo Kyeong

AU - Hwang, Eun Sook

N1 - Funding Information: We thank Dr. J. Alam (Alton Ochsner Medical Foundation, New Orleans) for providing pHO4.3k-luc vector and Ms. Hyun Jung Kim for helping histological analysis. This work was supported by the Basic research program ( 2012R1A1B3000603 for ESH and 2011-007983 for JOK) of the National Research Foundation funded by Ministry of Education, Science, and Technology.

PY - 2014/1/3

Y1 - 2014/1/3

N2 - Skeletal muscle plays key roles in metabolic homeostasis. Loss of muscle mass, called muscle atrophy exacerbates disease-associated metabolic perturbations. In this study, we characterized the molecular functions and mechanisms underlying regulation of skeletal muscle atrophy induced by denervation. Denervation significantly increased the expression of heme oxygenase-1 (HO-1) and atrogenes in skeletal muscle. Forkhead box protein O1 (FoxO1) drastically increased in atrophied muscle and selectively stimulated HO-1 gene transcription through direct DNA binding. Lack of HO-1 substantially attenuated muscle atrophy, whereas HO-1 overexpression caused muscle damage in vitro and in vivo. Collectively, HO-1 induced by FoxO1 may cause skeletal muscle atrophy.

AB - Skeletal muscle plays key roles in metabolic homeostasis. Loss of muscle mass, called muscle atrophy exacerbates disease-associated metabolic perturbations. In this study, we characterized the molecular functions and mechanisms underlying regulation of skeletal muscle atrophy induced by denervation. Denervation significantly increased the expression of heme oxygenase-1 (HO-1) and atrogenes in skeletal muscle. Forkhead box protein O1 (FoxO1) drastically increased in atrophied muscle and selectively stimulated HO-1 gene transcription through direct DNA binding. Lack of HO-1 substantially attenuated muscle atrophy, whereas HO-1 overexpression caused muscle damage in vitro and in vivo. Collectively, HO-1 induced by FoxO1 may cause skeletal muscle atrophy.

KW - FoxO1

KW - MAFbx

KW - MuRF1

KW - NRF2

KW - Nerve injury

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DO - 10.1016/j.febslet.2013.11.009

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SN - 0014-5793

VL - 588

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EP - 85

JO - FEBS Letters

JF - FEBS Letters

IS - 1

ER -

A FoxO1-dependent, but NRF2-independent induction of heme oxygenase-1 during muscle atrophy

Abstract

Keywords

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