Arsenite stabilizes IκBα and prevents NF-κB activation in IL-1 β-stimulated Caco-2 cells independent of the heat shock response

Dan D. Hershko, Bruce Robb, Eric S. Hungness, Guangju Luo, Per Olof Hasselgren

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Recent studies suggest that sodium arsenite downregulates NF-κB activity by inhibiting phosphorylation and subsequent degradation of IκBα. Many effects of sodium arsenite are secondary to induction of heat shock proteins. The role of the heat shock response in arsenite-induced inhibition of NF-κB, however, is not known. We examined the involvement of the heat shock response in arsenite-induced inhibition of NF-κB activity in IL-1 β-stimulated Caco-2 cells, a human colorectal adenocarcinoma cell line with enterocytic properties. Treatment of the cells with IL-1 B resulted in increased IκB kinase activity, reduced levels of IκBαand increased NF-κB DNA binding activity. Sodium arsenite blocked all of these responses to IL-1 β without inducing changes in heat shock factor activity or heat shock protein levels. Results from additional experiments showed that the protective effect of sodium arsenite on IκBα was not influenced by the oxygen radical scavenger catalase or by inhibitors of the MAP-kinase signaling pathway. The present results suggest that sodium arsenite stabilizes IκBαand prevents NF-κB activation in IL-1 β-stimulated Caco-2 cells independent of the heat shock response. In addition, stabilization of IκBα by sodium arsenite does not require oxygen radical formation or activation of the MAP kinase signaling pathway.

Original languageEnglish (US)
Pages (from-to)687-698
Number of pages12
JournalJournal of Cellular Biochemistry
Volume84
Issue number4
DOIs
StatePublished - 2002
Externally publishedYes

Fingerprint

Heat-Shock Response
Caco-2 Cells
Interleukin-1
Chemical activation
Phosphotransferases
MAP Kinase Signaling System
Heat-Shock Proteins
Reactive Oxygen Species
Cells
Phosphorylation
Catalase
sodium arsenite
arsenite
Hot Temperature
Shock
Adenocarcinoma
Down-Regulation
Stabilization
Cell Line
Degradation

Keywords

  • Cytokines
  • Inflammation
  • Intestine
  • Stress response

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

Cite this

Arsenite stabilizes IκBα and prevents NF-κB activation in IL-1 β-stimulated Caco-2 cells independent of the heat shock response. / Hershko, Dan D.; Robb, Bruce; Hungness, Eric S.; Luo, Guangju; Hasselgren, Per Olof.

In: Journal of Cellular Biochemistry, Vol. 84, No. 4, 2002, p. 687-698.

Research output: Contribution to journalArticle

Hershko, Dan D. ; Robb, Bruce ; Hungness, Eric S. ; Luo, Guangju ; Hasselgren, Per Olof. / Arsenite stabilizes IκBα and prevents NF-κB activation in IL-1 β-stimulated Caco-2 cells independent of the heat shock response. In: Journal of Cellular Biochemistry. 2002 ; Vol. 84, No. 4. pp. 687-698.
@article{71ac4547234347298deb27d1891522b5,
title = "Arsenite stabilizes IκBα and prevents NF-κB activation in IL-1 β-stimulated Caco-2 cells independent of the heat shock response",
abstract = "Recent studies suggest that sodium arsenite downregulates NF-κB activity by inhibiting phosphorylation and subsequent degradation of IκBα. Many effects of sodium arsenite are secondary to induction of heat shock proteins. The role of the heat shock response in arsenite-induced inhibition of NF-κB, however, is not known. We examined the involvement of the heat shock response in arsenite-induced inhibition of NF-κB activity in IL-1 β-stimulated Caco-2 cells, a human colorectal adenocarcinoma cell line with enterocytic properties. Treatment of the cells with IL-1 B resulted in increased IκB kinase activity, reduced levels of IκBαand increased NF-κB DNA binding activity. Sodium arsenite blocked all of these responses to IL-1 β without inducing changes in heat shock factor activity or heat shock protein levels. Results from additional experiments showed that the protective effect of sodium arsenite on IκBα was not influenced by the oxygen radical scavenger catalase or by inhibitors of the MAP-kinase signaling pathway. The present results suggest that sodium arsenite stabilizes IκBαand prevents NF-κB activation in IL-1 β-stimulated Caco-2 cells independent of the heat shock response. In addition, stabilization of IκBα by sodium arsenite does not require oxygen radical formation or activation of the MAP kinase signaling pathway.",
keywords = "Cytokines, Inflammation, Intestine, Stress response",
author = "Hershko, {Dan D.} and Bruce Robb and Hungness, {Eric S.} and Guangju Luo and Hasselgren, {Per Olof}",
year = "2002",
doi = "10.1002/jcb.10083",
language = "English (US)",
volume = "84",
pages = "687--698",
journal = "Journal of Cellular Biochemistry",
issn = "0730-2312",
publisher = "Wiley-Liss Inc.",
number = "4",

}

TY - JOUR

T1 - Arsenite stabilizes IκBα and prevents NF-κB activation in IL-1 β-stimulated Caco-2 cells independent of the heat shock response

AU - Hershko, Dan D.

AU - Robb, Bruce

AU - Hungness, Eric S.

AU - Luo, Guangju

AU - Hasselgren, Per Olof

PY - 2002

Y1 - 2002

N2 - Recent studies suggest that sodium arsenite downregulates NF-κB activity by inhibiting phosphorylation and subsequent degradation of IκBα. Many effects of sodium arsenite are secondary to induction of heat shock proteins. The role of the heat shock response in arsenite-induced inhibition of NF-κB, however, is not known. We examined the involvement of the heat shock response in arsenite-induced inhibition of NF-κB activity in IL-1 β-stimulated Caco-2 cells, a human colorectal adenocarcinoma cell line with enterocytic properties. Treatment of the cells with IL-1 B resulted in increased IκB kinase activity, reduced levels of IκBαand increased NF-κB DNA binding activity. Sodium arsenite blocked all of these responses to IL-1 β without inducing changes in heat shock factor activity or heat shock protein levels. Results from additional experiments showed that the protective effect of sodium arsenite on IκBα was not influenced by the oxygen radical scavenger catalase or by inhibitors of the MAP-kinase signaling pathway. The present results suggest that sodium arsenite stabilizes IκBαand prevents NF-κB activation in IL-1 β-stimulated Caco-2 cells independent of the heat shock response. In addition, stabilization of IκBα by sodium arsenite does not require oxygen radical formation or activation of the MAP kinase signaling pathway.

AB - Recent studies suggest that sodium arsenite downregulates NF-κB activity by inhibiting phosphorylation and subsequent degradation of IκBα. Many effects of sodium arsenite are secondary to induction of heat shock proteins. The role of the heat shock response in arsenite-induced inhibition of NF-κB, however, is not known. We examined the involvement of the heat shock response in arsenite-induced inhibition of NF-κB activity in IL-1 β-stimulated Caco-2 cells, a human colorectal adenocarcinoma cell line with enterocytic properties. Treatment of the cells with IL-1 B resulted in increased IκB kinase activity, reduced levels of IκBαand increased NF-κB DNA binding activity. Sodium arsenite blocked all of these responses to IL-1 β without inducing changes in heat shock factor activity or heat shock protein levels. Results from additional experiments showed that the protective effect of sodium arsenite on IκBα was not influenced by the oxygen radical scavenger catalase or by inhibitors of the MAP-kinase signaling pathway. The present results suggest that sodium arsenite stabilizes IκBαand prevents NF-κB activation in IL-1 β-stimulated Caco-2 cells independent of the heat shock response. In addition, stabilization of IκBα by sodium arsenite does not require oxygen radical formation or activation of the MAP kinase signaling pathway.

KW - Cytokines

KW - Inflammation

KW - Intestine

KW - Stress response

UR - http://www.scopus.com/inward/record.url?scp=0036007395&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036007395&partnerID=8YFLogxK

U2 - 10.1002/jcb.10083

DO - 10.1002/jcb.10083

M3 - Article

C2 - 11835394

AN - SCOPUS:0036007395

VL - 84

SP - 687

EP - 698

JO - Journal of Cellular Biochemistry

JF - Journal of Cellular Biochemistry

SN - 0730-2312

IS - 4

ER -