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Role of the JNK/c-Jun/AP-1 signaling pathway in galectin-1-induced T-cell death

B Brandt1, E F Abou-Eladab, M Tiedge

  • 1Medical Faculty, Department of Medical Biochemistry and Molecular Biology, University of Rostock, Rostock, Germany.

Cell Death & Disease
|March 3, 2011
PubMed

Insights

Galectin-1 (gal-1) activates the JNK/c-Jun/AP-1 pathway, leading to T-cell apoptosis. This study elucidates gal-1

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Galectin-1 (gal-1) is an endogenous lectin involved in T-cell apoptosis.
  • T-cell death can be mediated by death receptor and mitochondrial pathways.

Purpose of the Study:

  • To investigate the molecular mechanisms by which gal-1 induces T-cell death.
  • To identify the role of the JNK/c-Jun/AP-1 pathway in gal-1-mediated apoptosis.

Main Methods:

  • Jurkat T cells were treated with gal-1.
  • Inhibition of JNK, PKCδ, and PKCθ pathways using specific inhibitors.
  • Analysis of c-Jun phosphorylation, AP-1 activity, and Bcl-2 family protein expression.
  • Use of CD3-deficient Jurkat cells to assess T-cell receptor dependence.

Main Results:

  • Gal-1 activates c-Jun N-terminal kinase (JNK) via MKK4 and MKK7.
  • Ceramide and PKCδ/PKCθ phosphorylation mediate gal-1-induced JNK activation.
  • JNK activation leads to c-Jun phosphorylation and AP-1 DNA-binding activity.
  • Inhibition of JNK or AP-1 reduces gal-1-induced DNA fragmentation.
  • Gal-1 induces a proapoptotic signaling pattern, including altered Bcl-2 family protein expression.

Conclusions:

  • The JNK/c-Jun/AP-1 pathway is crucial for gal-1-induced T-cell apoptosis.
  • Gal-1-mediated T-cell death is partly dependent on T-cell receptor signaling.
  • These findings offer insights into T-cell death regulation by gal-1.

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