Regulatory mechanism of TNFα autoregulation in HaCaT cells: The role of the transcription factor EGR-1

Sang Wook Son; Byong Wook Min; Yoongho Lim; Young Han Lee; Soon Young Shin

doi:10.1016/j.bbrc.2008.07.117

Regulatory mechanism of TNFα autoregulation in HaCaT cells: The role of the transcription factor EGR-1

Sang Wook Son, Byong Wook Min, Yoongho Lim, Young Han Lee, Soon Young Shin

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

20 Citations (Scopus)

Abstract

Tumor necrosis factor α (TNFα) is a pro-inflammatory cytokine involved in innate immune response, as well as in the pathogenesis of many inflammatory diseases. Although several response elements in the TNFα promoter region are involved in the activation of gene transcription, few studies have examined the regulatory mechanism that controls TNFα autoregulation. In this study, we investigated the role of the Early Growth Response-1 (EGR-1) transcription factor in TNFα autoregulation in HaCaT human keratinocytes. The requirement for EGR-1 in TNFα autoregulation was confirmed using a construct harboring a point mutation in the EGR-1 binding site within the TNFα promoter and the introduction of EGR-1 siRNA. Inhibition of the ERK or JNK pathway suppressed TNFα-induced EGR-1 expression, resulting in the inhibition of TNFα-induced TNFα promoter activation. These results reveal that the ERK and JNK MAPK pathways contribute to the autoregulation of TNFα synthesis via EGR-1 induction in HaCaT keratinocytes.

Original language	English
Pages (from-to)	777-782
Number of pages	6
Journal	Biochemical and biophysical research communications
Volume	374
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2008.07.117
Publication status	Published - 2008 Oct 3

Keywords

Autoregulation
EGR-1
Mitogen-activated protein kinase
Tumor necrosis factor α

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following Sustainable Development Goal(s)

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title = "Regulatory mechanism of TNFα autoregulation in HaCaT cells: The role of the transcription factor EGR-1",

abstract = "Tumor necrosis factor α (TNFα) is a pro-inflammatory cytokine involved in innate immune response, as well as in the pathogenesis of many inflammatory diseases. Although several response elements in the TNFα promoter region are involved in the activation of gene transcription, few studies have examined the regulatory mechanism that controls TNFα autoregulation. In this study, we investigated the role of the Early Growth Response-1 (EGR-1) transcription factor in TNFα autoregulation in HaCaT human keratinocytes. The requirement for EGR-1 in TNFα autoregulation was confirmed using a construct harboring a point mutation in the EGR-1 binding site within the TNFα promoter and the introduction of EGR-1 siRNA. Inhibition of the ERK or JNK pathway suppressed TNFα-induced EGR-1 expression, resulting in the inhibition of TNFα-induced TNFα promoter activation. These results reveal that the ERK and JNK MAPK pathways contribute to the autoregulation of TNFα synthesis via EGR-1 induction in HaCaT keratinocytes.",

keywords = "Autoregulation, EGR-1, Mitogen-activated protein kinase, Tumor necrosis factor α",

author = "Son, {Sang Wook} and Min, {Byong Wook} and Yoongho Lim and Lee, {Young Han} and Shin, {Soon Young}",

note = "Funding Information: This study was supported by the Disease Network Research Program from the Korea Science & Engineering Foundation (KOSEF), funded by the Korean Government (Grant No. M10751050003-07N5105-00310). Copyright: Copyright 2008 Elsevier B.V., All rights reserved.",

year = "2008",

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doi = "10.1016/j.bbrc.2008.07.117",

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AU - Lee, Young Han

AU - Shin, Soon Young

N1 - Funding Information: This study was supported by the Disease Network Research Program from the Korea Science & Engineering Foundation (KOSEF), funded by the Korean Government (Grant No. M10751050003-07N5105-00310). Copyright: Copyright 2008 Elsevier B.V., All rights reserved.

PY - 2008/10/3

Y1 - 2008/10/3

N2 - Tumor necrosis factor α (TNFα) is a pro-inflammatory cytokine involved in innate immune response, as well as in the pathogenesis of many inflammatory diseases. Although several response elements in the TNFα promoter region are involved in the activation of gene transcription, few studies have examined the regulatory mechanism that controls TNFα autoregulation. In this study, we investigated the role of the Early Growth Response-1 (EGR-1) transcription factor in TNFα autoregulation in HaCaT human keratinocytes. The requirement for EGR-1 in TNFα autoregulation was confirmed using a construct harboring a point mutation in the EGR-1 binding site within the TNFα promoter and the introduction of EGR-1 siRNA. Inhibition of the ERK or JNK pathway suppressed TNFα-induced EGR-1 expression, resulting in the inhibition of TNFα-induced TNFα promoter activation. These results reveal that the ERK and JNK MAPK pathways contribute to the autoregulation of TNFα synthesis via EGR-1 induction in HaCaT keratinocytes.

AB - Tumor necrosis factor α (TNFα) is a pro-inflammatory cytokine involved in innate immune response, as well as in the pathogenesis of many inflammatory diseases. Although several response elements in the TNFα promoter region are involved in the activation of gene transcription, few studies have examined the regulatory mechanism that controls TNFα autoregulation. In this study, we investigated the role of the Early Growth Response-1 (EGR-1) transcription factor in TNFα autoregulation in HaCaT human keratinocytes. The requirement for EGR-1 in TNFα autoregulation was confirmed using a construct harboring a point mutation in the EGR-1 binding site within the TNFα promoter and the introduction of EGR-1 siRNA. Inhibition of the ERK or JNK pathway suppressed TNFα-induced EGR-1 expression, resulting in the inhibition of TNFα-induced TNFα promoter activation. These results reveal that the ERK and JNK MAPK pathways contribute to the autoregulation of TNFα synthesis via EGR-1 induction in HaCaT keratinocytes.

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Regulatory mechanism of TNFα autoregulation in HaCaT cells: The role of the transcription factor EGR-1

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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