NF-κB activates fibronectin gene expression in rat hepatocytes

Byung Heon Lee; Seung Yoon Park; Kae Bok Kang; Rang Woon Park; In San Kim

doi:10.1016/S0006-291X(02)02356-2

NF-κB activates fibronectin gene expression in rat hepatocytes

Byung Heon Lee, Seung Yoon Park, Kae Bok Kang, Rang Woon Park, In San Kim

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

38 Citations (Scopus)

Abstract

Fibronectin (FN) plays a role in various biological processes such as fibrosis and tumor metastasis. In this study, we investigated the regulation of FN gene expression by NF-κB transcription factor. Transient expression of NF-κB p65 increased FN promoter activity in rat hepatocytes. Deletion analysis of FN promoter localized the NF-κB-responsive region at the position between -1214 and -1126. Mutations in a putative NF-κB element (5′-GAGAATTTCC-3′) at -1180 blocked most of the p65-induced promoter activity. Electromobility shift assays showed that the expression of p65 induced the binding of the p65/p65 homodimer to the NF-κB site at -1180. Stably p65-expressing cells showed increase of promoter activity, FN protein, and its mRNA levels over control cells. Furthermore, treatment of cells with interleukin-1β, a NF-κB-stimulating cytokine, also increased promoter activity, FN production, and mRNA levels. These results show that NF-κB activates FN gene expression by binding to the responsive element at -1180 as the p65/p65 homodimer in rat hepatocytes.

Original language	English
Pages (from-to)	1218-1224
Number of pages	7
Journal	Biochemical and biophysical research communications
Volume	297
Issue number	5
DOIs	https://doi.org/10.1016/S0006-291X(02)02356-2
Publication status	Published - 2002
Externally published	Yes

Bibliographical note

Funding Information:
We thank Dr. Kinichiro Oda (Science University of Tokyo, Tokyo, Japan) for providing pF882CAT construct and Dr. Patrick A Baeuerle (Tularik, South San Francisco, A) for pCMV-p65 expression vector. This work was supported by a program of National Research Laboratory (M10104000036-01J0000-01610).

Keywords

Fibronectin
Hepatocyte
NF-κB

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/S0006-291X(02)02356-2

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title = "NF-κB activates fibronectin gene expression in rat hepatocytes",

abstract = "Fibronectin (FN) plays a role in various biological processes such as fibrosis and tumor metastasis. In this study, we investigated the regulation of FN gene expression by NF-κB transcription factor. Transient expression of NF-κB p65 increased FN promoter activity in rat hepatocytes. Deletion analysis of FN promoter localized the NF-κB-responsive region at the position between -1214 and -1126. Mutations in a putative NF-κB element (5′-GAGAATTTCC-3′) at -1180 blocked most of the p65-induced promoter activity. Electromobility shift assays showed that the expression of p65 induced the binding of the p65/p65 homodimer to the NF-κB site at -1180. Stably p65-expressing cells showed increase of promoter activity, FN protein, and its mRNA levels over control cells. Furthermore, treatment of cells with interleukin-1β, a NF-κB-stimulating cytokine, also increased promoter activity, FN production, and mRNA levels. These results show that NF-κB activates FN gene expression by binding to the responsive element at -1180 as the p65/p65 homodimer in rat hepatocytes.",

keywords = "Fibronectin, Hepatocyte, NF-κB",

author = "Lee, {Byung Heon} and Park, {Seung Yoon} and Kang, {Kae Bok} and Park, {Rang Woon} and Kim, {In San}",

note = "Funding Information: We thank Dr. Kinichiro Oda (Science University of Tokyo, Tokyo, Japan) for providing pF882CAT construct and Dr. Patrick A Baeuerle (Tularik, South San Francisco, A) for pCMV-p65 expression vector. This work was supported by a program of National Research Laboratory (M10104000036-01J0000-01610).",

year = "2002",

doi = "10.1016/S0006-291X(02)02356-2",

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T1 - NF-κB activates fibronectin gene expression in rat hepatocytes

AU - Lee, Byung Heon

AU - Park, Seung Yoon

AU - Kang, Kae Bok

AU - Park, Rang Woon

AU - Kim, In San

N1 - Funding Information: We thank Dr. Kinichiro Oda (Science University of Tokyo, Tokyo, Japan) for providing pF882CAT construct and Dr. Patrick A Baeuerle (Tularik, South San Francisco, A) for pCMV-p65 expression vector. This work was supported by a program of National Research Laboratory (M10104000036-01J0000-01610).

PY - 2002

Y1 - 2002

N2 - Fibronectin (FN) plays a role in various biological processes such as fibrosis and tumor metastasis. In this study, we investigated the regulation of FN gene expression by NF-κB transcription factor. Transient expression of NF-κB p65 increased FN promoter activity in rat hepatocytes. Deletion analysis of FN promoter localized the NF-κB-responsive region at the position between -1214 and -1126. Mutations in a putative NF-κB element (5′-GAGAATTTCC-3′) at -1180 blocked most of the p65-induced promoter activity. Electromobility shift assays showed that the expression of p65 induced the binding of the p65/p65 homodimer to the NF-κB site at -1180. Stably p65-expressing cells showed increase of promoter activity, FN protein, and its mRNA levels over control cells. Furthermore, treatment of cells with interleukin-1β, a NF-κB-stimulating cytokine, also increased promoter activity, FN production, and mRNA levels. These results show that NF-κB activates FN gene expression by binding to the responsive element at -1180 as the p65/p65 homodimer in rat hepatocytes.

AB - Fibronectin (FN) plays a role in various biological processes such as fibrosis and tumor metastasis. In this study, we investigated the regulation of FN gene expression by NF-κB transcription factor. Transient expression of NF-κB p65 increased FN promoter activity in rat hepatocytes. Deletion analysis of FN promoter localized the NF-κB-responsive region at the position between -1214 and -1126. Mutations in a putative NF-κB element (5′-GAGAATTTCC-3′) at -1180 blocked most of the p65-induced promoter activity. Electromobility shift assays showed that the expression of p65 induced the binding of the p65/p65 homodimer to the NF-κB site at -1180. Stably p65-expressing cells showed increase of promoter activity, FN protein, and its mRNA levels over control cells. Furthermore, treatment of cells with interleukin-1β, a NF-κB-stimulating cytokine, also increased promoter activity, FN production, and mRNA levels. These results show that NF-κB activates FN gene expression by binding to the responsive element at -1180 as the p65/p65 homodimer in rat hepatocytes.

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NF-κB activates fibronectin gene expression in rat hepatocytes

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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