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Apoptosis signal-regulating kinase 1 regulates the expression of caspase-11

Jong-Ryoul Choi1, Hyejung Heo, Yoo Lang

  • 1Department of Molecular Biology, Sejong University, Seoul 143-747, Republic of Korea.

FEBS Letters
|August 22, 2009
PubMed

Insights

Lipopolysaccharide (LPS) induces caspase-11 expression via the apoptosis signal-regulating kinase 1 (Ask1) pathway. This study reveals Ask1

Area of Science:

  • Immunology
  • Cellular Biology
  • Molecular Signaling

Background:

  • Caspase-11 is a key regulator of inflammation and cell death.
  • Lipopolysaccharide (LPS) is a potent immune activator.
  • The signaling pathways upstream of caspase-11 induction remain incompletely understood.

Purpose of the Study:

  • To investigate the role of the apoptosis signal-regulating kinase 1 (Ask1) pathway in LPS-induced caspase-11 expression.
  • To identify upstream mediators of Ask1 activation in response to LPS.

Main Methods:

  • Utilized inhibitors of NADPH oxidase (Nox) and small interfering RNA (siRNA) for Nox4 knockdown.
  • Employed dominant-negative constructs for tumor necrosis factor receptor-associated factor 6 (TRAF6) and Ask1.
  • Assessed caspase-11 induction following LPS stimulation in various experimental conditions.

Main Results:

  • NADPH oxidase (Nox) and specifically Nox4 were found to be essential for LPS-induced caspase-11 expression.
  • Reactive oxygen species (ROS) generated by Nox4 activate the Ask1 pathway.
  • Inhibition or knockdown of Ask1 significantly suppressed caspase-11 induction by LPS.
  • TRAF6 signaling also plays a role in the regulation of caspase-11 induction.

Conclusions:

  • The Ask1-mediated signaling pathway, activated by ROS from Nox4, is crucial for the induction of caspase-11 by LPS.
  • This finding elucidates a novel regulatory mechanism for caspase-11 expression in innate immunity.

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