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RelB/p50 complexes regulate cytokine-induced YKL-40 expression.

Reetika Bhardwaj1, Jessie W Yester1, Sandeep K Singh1

  • 1Department of Biochemistry and Molecular Biology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298;

Journal of Immunology (Baltimore, Md. : 1950)
|February 15, 2015
PubMed
Summary
This summary is machine-generated.

Researchers discovered that Interleukin-1 (IL-1) and Interleukin-6 (IL-6) family cytokines drive YKL-40 expression in astrocytes. This involves STAT3 and a non-canonical NF-κB pathway (RelB/p50), offering insights into inflammatory gene regulation.

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Area of Science:

  • Neuroimmunology
  • Molecular Biology
  • Inflammation Research

Background:

  • YKL-40 is a biomarker for inflammatory diseases like multiple sclerosis and Alzheimer's.
  • The molecular mechanisms and inflammatory mediators controlling YKL-40 expression were previously unknown.

Purpose of the Study:

  • To elucidate the inflammatory mediators and molecular mechanisms regulating YKL-40 expression in astrocytes.
  • To investigate the role of specific signaling pathways in cytokine-induced YKL-40 upregulation.

Main Methods:

  • Utilized mouse models of inflammation and primary human/mouse astrocyte cultures.
  • Analyzed gene expression, promoter binding assays, and utilized genetic manipulation (constitutively active STAT3, dominant-negative IκBα).
  • Investigated the involvement of STAT3, NF-κB subunits (p65, RelB, p50), IL-1, IL-6, and oncostatin M.

Main Results:

  • YKL-40 expression correlated with IL-1 and IL-6 levels in vivo.
  • IL-1 and IL-6 family cytokines synergistically upregulated YKL-40 in astrocytes.
  • Cytokine-driven YKL-40 expression required STAT3 and NF-κB binding elements, specifically involving RelB/p50 complexes, not p65.
  • Oncostatin M enhanced IL-1-induced RelB/p50 complex formation that bound to the YKL-40 promoter.

Conclusions:

  • IL-1 and IL-6 family cytokines regulate YKL-40 expression in astrocytes via STAT3 and RelB/p50 complexes during sterile inflammation.
  • The findings reveal a novel mechanism for inflammatory gene regulation involving non-canonical NF-κB activation.
  • Suggests IL-1 may control anti-inflammatory gene expression in nonlymphoid tissues through RelB/p50 activation.