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PMID: 2557635 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Induction of the transcription factor IRF-1 and interferon-beta mRNAs by cytokines and activators of second-messenger pathways.

Proceedings of the National Academy of Sciences of the United States of America ·Vol. 86 ·No. 24 ·1989-12-00 ·Pages 9936-40

Fujita T, Reis LF, Watanabe N, Kimura Y, Taniguchi T, Vilcek J

Abstract

Nuclear protein IRF-1 (interferon regulatory factor 1) was earlier shown to bind to cis-acting regulatory elements present on interferon (IFN)-alpha/beta genes and some IFN-inducible genes. Here we show that in both human FS-4 and murine L929 cells, steady-state levels of IRF-1 mRNA were increased by treatment with tumor necrosis factor (TNF), interleukin 1 (IL-1), poly(I).poly(C), or IFN-beta. IRF-1 mRNA induction was also demonstrated in cells treated with calcium ionophore A23187 or with phorbol 12-myristate 13-acetate, but not with epidermal growth factor, dibutyryl-cAMP, or the adenylate cyclase activator forskolin. To determine whether stimulation of IRF-1 mRNA levels correlates with IFN-beta induction, we compared IRF-1 and IFN-beta mRNA levels in cells exposed to various stimuli. In L929 cells, treatment with poly(I).poly(C) under conditions that failed to induce significant levels of IFN-beta mRNA led to a very low induction of IRF-1 mRNA, but "priming" cells with IFN prior to the addition of poly(I).poly(C) greatly increased both IRF-1 and IFN-beta mRNAs. In FS-4 cells an increase in IFN-beta mRNA (examined by the polymerase chain reaction) was seen after treatment with TNF, IL-1, A23187, or poly(I).poly(C), but not with IFN-beta, epidermal growth factor, dibutyryl-cAMP, or forskolin. Thus, all treatments that increased steady-state levels of IFN-beta mRNA also enhanced IRF-1 mRNA levels. However, treatment with IFN-beta, which caused a marked stimulation in IRF-1 mRNA, failed to produce a detectable increase in IFN-beta mRNA. It appears that IRF-1 may be necessary but not sufficient for IFN-beta induction. The ability of TNF and IL-1 to increase both IRF-1 and IFN-beta mRNAs may be responsible for some similarities in the actions of TNF, IL-1, and the IFNs.

MeSH Terms
Animals Base Sequence Biological Factors/pharmacology Blotting, Northern Bucladesine/pharmacology Calcimycin/pharmacology Cell Line Colforsin/pharmacology Cytokines DNA-Binding Proteins/genetics DNA-Directed DNA Polymerase Humans Interferon Regulatory Factor-1 Interferon-gamma/genetics Interleukin-1/pharmacology Kinetics L Cells/immunology Mice Molecular Sequence Data Oligonucleotide Probes Phosphoproteins Polymerase Chain Reaction RNA, Messenger/analysis,biosynthesis,genetics Recombinant Proteins/pharmacology Second Messenger Systems/drug effects Taq Polymerase Tetradecanoylphorbol Acetate/pharmacology Transcription Factors/genetics Transcription, Genetic/drug effects Tumor Necrosis Factor-alpha/pharmacology
Chemicals
Biological Factors Cytokines DNA-Binding Proteins IRF1 protein, human Interferon Regulatory Factor-1 Interleukin-1 Irf1 protein, mouse Oligonucleotide Probes Phosphoproteins RNA, Messenger Recombinant Proteins Transcription Factors Tumor Necrosis Factor-alpha Colforsin Calcimycin Bucladesine Interferon-gamma Taq Polymerase DNA-Directed DNA Polymerase Tetradecanoylphorbol Acetate
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Fujita T
Institute for Molecular and Cellular Biology, Osaka University, Japan.
Reis L F
Watanabe N
Kimura Y
Taniguchi T
Vilcek J
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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
DOI
10.1073/pnas.86.24.9936
Published
1989-12-00
Pages
9936-40
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC298617
Subset
IM
Grants
NIAID NIH HHS · AI12948 · United States
NCI NIH HHS · CA47301 · United States
External Links
PubMed source DOI: 10.1073/pnas.86.24.9936 PMC Full Text View journal details
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