Mechanism of interleukin-1α transcriptional regulation of S100A9 in a human epidermal keratinocyte cell line

Mika Bando, Xianqiong Zou, Yuka Hiroshima, Masatoshi Kataoka, Karen F. Ross, Yasuo Shinohara, Toshihiko Nagata, Mark C. Herzberg, Jun ichi Kido

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

S100A9 is a calcium-binding protein and subunit of antimicrobial calprotectin complex (S100A8/A9). Produced by neutrophils, monocytes/macrophages and keratinocytes, S100A9 expression increases in response to inflammation. For example, IL-1α produced by epithelial cells acts autonomously on the same cells to induce the expression of S100A8/A9 and cellular differentiation. Whereas it is well known that IL-1α and members of the IL-10 family of cytokines upregulate S100A8 and S100A9 in several cell lineages, the pathway and mechanism of IL-1α-dependent transcriptional control of S100A9 in epithelial cells are not established. Modeled using human epidermal keratinocytes (HaCaT cells), IL-1α stimulated the phosphorylation of p38 MAPK and induced S100A9 expression, which was blocked by IL-1 receptor antagonist, RNAi suppression of p38, or a p38 MAPK inhibitor. Transcription of S100A9 in HaCaT cells depended on nucleotides -. 94 to -. 53 in the upstream promoter region, based upon the use of deletion constructs and luciferase reporter activity. Within the responsive promoter region, IL-1α increased the binding activity of CCAAT/enhancer binding protein β (C/EBPβ). Mutated C/EBPβ binding sequences or C/EBPβ-specific siRNA inhibited the S100A9 transcriptional response. Hence, IL-1α is strongly suggested to increase S100A9 expression in a human epidermal keratinocyte cell line by signaling through the IL-1 receptor and p38 MAPK, increasing C/EBPβ-dependent transcriptional activity.

Original languageEnglish (US)
Pages (from-to)954-962
Number of pages9
JournalBiochimica et Biophysica Acta - Gene Regulatory Mechanisms
Volume1829
Issue number9
DOIs
StatePublished - Sep 1 2013

Fingerprint

Interleukin-1
Keratinocytes
CCAAT-Enhancer-Binding Proteins
Cells
Cell Line
p38 Mitogen-Activated Protein Kinases
Interleukin-1 Receptors
Genetic Promoter Regions
Epithelial Cells
Leukocyte L1 Antigen Complex
Phosphorylation
Calcium-Binding Proteins
Macrophages
Protein Subunits
Cell Lineage
Transcription
RNA Interference
Luciferases
Protein Binding
Interleukin-10

Keywords

  • C/EBPβ
  • IL-1α
  • Keratinocytes
  • P38
  • S100A9

Cite this

Mechanism of interleukin-1α transcriptional regulation of S100A9 in a human epidermal keratinocyte cell line. / Bando, Mika; Zou, Xianqiong; Hiroshima, Yuka; Kataoka, Masatoshi; Ross, Karen F.; Shinohara, Yasuo; Nagata, Toshihiko; Herzberg, Mark C.; Kido, Jun ichi.

In: Biochimica et Biophysica Acta - Gene Regulatory Mechanisms, Vol. 1829, No. 9, 01.09.2013, p. 954-962.

Research output: Contribution to journalArticle

Bando, Mika ; Zou, Xianqiong ; Hiroshima, Yuka ; Kataoka, Masatoshi ; Ross, Karen F. ; Shinohara, Yasuo ; Nagata, Toshihiko ; Herzberg, Mark C. ; Kido, Jun ichi. / Mechanism of interleukin-1α transcriptional regulation of S100A9 in a human epidermal keratinocyte cell line. In: Biochimica et Biophysica Acta - Gene Regulatory Mechanisms. 2013 ; Vol. 1829, No. 9. pp. 954-962.
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AU - Bando, Mika

AU - Zou, Xianqiong

AU - Hiroshima, Yuka

AU - Kataoka, Masatoshi

AU - Ross, Karen F.

AU - Shinohara, Yasuo

AU - Nagata, Toshihiko

AU - Herzberg, Mark C.

AU - Kido, Jun ichi

PY - 2013/9/1

Y1 - 2013/9/1

N2 - S100A9 is a calcium-binding protein and subunit of antimicrobial calprotectin complex (S100A8/A9). Produced by neutrophils, monocytes/macrophages and keratinocytes, S100A9 expression increases in response to inflammation. For example, IL-1α produced by epithelial cells acts autonomously on the same cells to induce the expression of S100A8/A9 and cellular differentiation. Whereas it is well known that IL-1α and members of the IL-10 family of cytokines upregulate S100A8 and S100A9 in several cell lineages, the pathway and mechanism of IL-1α-dependent transcriptional control of S100A9 in epithelial cells are not established. Modeled using human epidermal keratinocytes (HaCaT cells), IL-1α stimulated the phosphorylation of p38 MAPK and induced S100A9 expression, which was blocked by IL-1 receptor antagonist, RNAi suppression of p38, or a p38 MAPK inhibitor. Transcription of S100A9 in HaCaT cells depended on nucleotides -. 94 to -. 53 in the upstream promoter region, based upon the use of deletion constructs and luciferase reporter activity. Within the responsive promoter region, IL-1α increased the binding activity of CCAAT/enhancer binding protein β (C/EBPβ). Mutated C/EBPβ binding sequences or C/EBPβ-specific siRNA inhibited the S100A9 transcriptional response. Hence, IL-1α is strongly suggested to increase S100A9 expression in a human epidermal keratinocyte cell line by signaling through the IL-1 receptor and p38 MAPK, increasing C/EBPβ-dependent transcriptional activity.

AB - S100A9 is a calcium-binding protein and subunit of antimicrobial calprotectin complex (S100A8/A9). Produced by neutrophils, monocytes/macrophages and keratinocytes, S100A9 expression increases in response to inflammation. For example, IL-1α produced by epithelial cells acts autonomously on the same cells to induce the expression of S100A8/A9 and cellular differentiation. Whereas it is well known that IL-1α and members of the IL-10 family of cytokines upregulate S100A8 and S100A9 in several cell lineages, the pathway and mechanism of IL-1α-dependent transcriptional control of S100A9 in epithelial cells are not established. Modeled using human epidermal keratinocytes (HaCaT cells), IL-1α stimulated the phosphorylation of p38 MAPK and induced S100A9 expression, which was blocked by IL-1 receptor antagonist, RNAi suppression of p38, or a p38 MAPK inhibitor. Transcription of S100A9 in HaCaT cells depended on nucleotides -. 94 to -. 53 in the upstream promoter region, based upon the use of deletion constructs and luciferase reporter activity. Within the responsive promoter region, IL-1α increased the binding activity of CCAAT/enhancer binding protein β (C/EBPβ). Mutated C/EBPβ binding sequences or C/EBPβ-specific siRNA inhibited the S100A9 transcriptional response. Hence, IL-1α is strongly suggested to increase S100A9 expression in a human epidermal keratinocyte cell line by signaling through the IL-1 receptor and p38 MAPK, increasing C/EBPβ-dependent transcriptional activity.

KW - C/EBPβ

KW - IL-1α

KW - Keratinocytes

KW - P38

KW - S100A9

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