Inhibition of cyclooxygenase-2 gene expression by the heat shock response in J774 murine macrophages

Armando Ialenti; Paola Di Meglio; Fulvio D'Acquisto; Barbara Pisano; Pasquale Maffia; Gianluca Grassia; Massimo Di Rosa; Angela Ianaro

doi:10.1016/j.ejphar.2004.10.052

Inhibition of cyclooxygenase-2 gene expression by the heat shock response in J774 murine macrophages

Armando Ialenti, Paola Di Meglio, Fulvio D'Acquisto, Barbara Pisano, Pasquale Maffia, Gianluca Grassia, Massimo Di Rosa, Angela Ianaro

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

Abstract

The heat shock response is a highly conserved mechanism of protection elicited in the cell by various kinds of stimuli, such as heat, sodium arsenite, oxidants and inflammation. Among the mechanisms potentially involved in mediating the protective effects of hsp, one of the most investigated is the inhibition of pro-inflammatory gene expression such as inducible nitric oxide synthase (iNOS) and inflammatory cytokines. Nevertheless, data about the effects of heat shock response on cyclooxygenase-2 expression in activated macrophages are so far not available in literature. The aim of this study was to investigate the changes in cyclooxygenase-2 expression following lipopolysaccharide stimulation of heat shocked J774 murine macrophages. We found, by Western blotting analysis and reverse transcription-polymerase chain reaction analysis (RT-PCR), that the lipopolysaccharide-induced cyclooxygenase-2 gene expression was reduced in heat shocked cells. Such a reduction was associated to activation of heat shock factor, increased levels of heat shock protein 72 and inhibition of lipopolysaccharide-induced nuclear factor-kappaB binding activity. These data suggest that the heat shock response inhibits cyclooxygenase-2 gene expression at transcriptional level, i.e. by preventing the activation of nuclear factor-kappaB, and provide additional information about mechanism(s) underlying the anti-inflammatory effect of the heat shock proteins.

Original language	English
Pages (from-to)	89-96
Number of pages	8
Journal	European journal of pharmacology
Volume	509
Issue number	2-3
DOIs	https://doi.org/10.1016/j.ejphar.2004.10.052
Publication status	Published - 21 Feb 2005

Keywords

Animals
Blotting, Western
Cell Line
Cyclooxygenase 2
DNA-Binding Proteins
Dinoprostone
Electrophoretic Mobility Shift Assay
Gene Expression Regulation, Enzymologic
HSP72 Heat-Shock Proteins
Heat Shock Transcription Factors
Heat-Shock Proteins
Heat-Shock Response
Lipopolysaccharides
Macrophages
Mice
NF-kappa B
Prostaglandin-Endoperoxide Synthases
Protein Binding
RNA, Messenger
Reverse Transcriptase Polymerase Chain Reaction
Transcription Factors
Comparative Study
Journal Article

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10.1016/j.ejphar.2004.10.052

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@article{b560225f85064d20baa2244b682abf22,

title = "Inhibition of cyclooxygenase-2 gene expression by the heat shock response in J774 murine macrophages",

abstract = "The heat shock response is a highly conserved mechanism of protection elicited in the cell by various kinds of stimuli, such as heat, sodium arsenite, oxidants and inflammation. Among the mechanisms potentially involved in mediating the protective effects of hsp, one of the most investigated is the inhibition of pro-inflammatory gene expression such as inducible nitric oxide synthase (iNOS) and inflammatory cytokines. Nevertheless, data about the effects of heat shock response on cyclooxygenase-2 expression in activated macrophages are so far not available in literature. The aim of this study was to investigate the changes in cyclooxygenase-2 expression following lipopolysaccharide stimulation of heat shocked J774 murine macrophages. We found, by Western blotting analysis and reverse transcription-polymerase chain reaction analysis (RT-PCR), that the lipopolysaccharide-induced cyclooxygenase-2 gene expression was reduced in heat shocked cells. Such a reduction was associated to activation of heat shock factor, increased levels of heat shock protein 72 and inhibition of lipopolysaccharide-induced nuclear factor-kappaB binding activity. These data suggest that the heat shock response inhibits cyclooxygenase-2 gene expression at transcriptional level, i.e. by preventing the activation of nuclear factor-kappaB, and provide additional information about mechanism(s) underlying the anti-inflammatory effect of the heat shock proteins.",

keywords = "Animals, Blotting, Western, Cell Line, Cyclooxygenase 2, DNA-Binding Proteins, Dinoprostone, Electrophoretic Mobility Shift Assay, Gene Expression Regulation, Enzymologic, HSP72 Heat-Shock Proteins, Heat Shock Transcription Factors, Heat-Shock Proteins, Heat-Shock Response, Lipopolysaccharides, Macrophages, Mice, NF-kappa B, Prostaglandin-Endoperoxide Synthases, Protein Binding, RNA, Messenger, Reverse Transcriptase Polymerase Chain Reaction, Transcription Factors, Comparative Study, Journal Article",

author = "Armando Ialenti and {Di Meglio}, Paola and Fulvio D'Acquisto and Barbara Pisano and Pasquale Maffia and Gianluca Grassia and {Di Rosa}, Massimo and Angela Ianaro",

year = "2005",

month = feb,

day = "21",

doi = "10.1016/j.ejphar.2004.10.052",

language = "English",

volume = "509",

pages = "89--96",

journal = "European journal of pharmacology",

issn = "0014-2999",

publisher = "Elsevier",

number = "2-3",

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TY - JOUR

T1 - Inhibition of cyclooxygenase-2 gene expression by the heat shock response in J774 murine macrophages

AU - Ialenti, Armando

AU - Di Meglio, Paola

AU - D'Acquisto, Fulvio

AU - Pisano, Barbara

AU - Maffia, Pasquale

AU - Grassia, Gianluca

AU - Di Rosa, Massimo

AU - Ianaro, Angela

PY - 2005/2/21

Y1 - 2005/2/21

N2 - The heat shock response is a highly conserved mechanism of protection elicited in the cell by various kinds of stimuli, such as heat, sodium arsenite, oxidants and inflammation. Among the mechanisms potentially involved in mediating the protective effects of hsp, one of the most investigated is the inhibition of pro-inflammatory gene expression such as inducible nitric oxide synthase (iNOS) and inflammatory cytokines. Nevertheless, data about the effects of heat shock response on cyclooxygenase-2 expression in activated macrophages are so far not available in literature. The aim of this study was to investigate the changes in cyclooxygenase-2 expression following lipopolysaccharide stimulation of heat shocked J774 murine macrophages. We found, by Western blotting analysis and reverse transcription-polymerase chain reaction analysis (RT-PCR), that the lipopolysaccharide-induced cyclooxygenase-2 gene expression was reduced in heat shocked cells. Such a reduction was associated to activation of heat shock factor, increased levels of heat shock protein 72 and inhibition of lipopolysaccharide-induced nuclear factor-kappaB binding activity. These data suggest that the heat shock response inhibits cyclooxygenase-2 gene expression at transcriptional level, i.e. by preventing the activation of nuclear factor-kappaB, and provide additional information about mechanism(s) underlying the anti-inflammatory effect of the heat shock proteins.

AB - The heat shock response is a highly conserved mechanism of protection elicited in the cell by various kinds of stimuli, such as heat, sodium arsenite, oxidants and inflammation. Among the mechanisms potentially involved in mediating the protective effects of hsp, one of the most investigated is the inhibition of pro-inflammatory gene expression such as inducible nitric oxide synthase (iNOS) and inflammatory cytokines. Nevertheless, data about the effects of heat shock response on cyclooxygenase-2 expression in activated macrophages are so far not available in literature. The aim of this study was to investigate the changes in cyclooxygenase-2 expression following lipopolysaccharide stimulation of heat shocked J774 murine macrophages. We found, by Western blotting analysis and reverse transcription-polymerase chain reaction analysis (RT-PCR), that the lipopolysaccharide-induced cyclooxygenase-2 gene expression was reduced in heat shocked cells. Such a reduction was associated to activation of heat shock factor, increased levels of heat shock protein 72 and inhibition of lipopolysaccharide-induced nuclear factor-kappaB binding activity. These data suggest that the heat shock response inhibits cyclooxygenase-2 gene expression at transcriptional level, i.e. by preventing the activation of nuclear factor-kappaB, and provide additional information about mechanism(s) underlying the anti-inflammatory effect of the heat shock proteins.

KW - Animals

KW - Blotting, Western

KW - Cell Line

KW - Cyclooxygenase 2

KW - DNA-Binding Proteins

KW - Dinoprostone

KW - Electrophoretic Mobility Shift Assay

KW - Gene Expression Regulation, Enzymologic

KW - HSP72 Heat-Shock Proteins

KW - Heat Shock Transcription Factors

KW - Heat-Shock Proteins

KW - Heat-Shock Response

KW - Lipopolysaccharides

KW - Macrophages

KW - Mice

KW - NF-kappa B

KW - Prostaglandin-Endoperoxide Synthases

KW - Protein Binding

KW - RNA, Messenger

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Transcription Factors

KW - Comparative Study

KW - Journal Article

U2 - 10.1016/j.ejphar.2004.10.052

DO - 10.1016/j.ejphar.2004.10.052

M3 - Article

C2 - 15733543

SN - 0014-2999

VL - 509

SP - 89

EP - 96

JO - European journal of pharmacology

JF - European journal of pharmacology

IS - 2-3

ER -