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Interleukin-13/Interleukin-4-induced oxidative stress contributes to death of prothrombinkringle-2 (pKr-2)-activated

So-Yoon Won1, Sang Ryong Kim, Sungho Maeng

  • 1Department of Biochemistry and Medical Research Center, Chungbuk National University College of Medicine, Cheongju 361-763, South Korea.

Journal of Neuroimmunology
|October 5, 2013
PubMed

Insights

Interleukin-13 (IL-13) and IL-4 induce microglia cell death via prothrombin kringle-2 (pKr-2) by increasing reactive oxygen species (ROS) and cyclooxygenase-2 (COX-2) expression. Oxidative stress and COX-2 activation contribute to this cell death.

Area of Science:

  • Neuroimmunology
  • Cell Biology
  • Biochemistry

Background:

  • Microglia play crucial roles in brain immunity and disease.
  • Prothrombin kringle-2 (pKr-2) is a distinct domain of prothrombin.
  • Interleukin-13 (IL-13) and IL-4 are anti-inflammatory cytokines.

Purpose of the Study:

  • To investigate if IL-13 or IL-4 induce cell death in activated microglia treated with pKr-2.
  • To elucidate the mechanisms underlying pKr-2 and cytokine-induced microglia cell death.

Main Methods:

  • In vitro co-treatment of activated microglia with pKr-2 and IL-13/IL-4.
  • Assessment of cell death using live/dead assays, TUNEL, and MTT assays.
  • Measurement of reactive oxygen species (ROS) and cyclooxygenase-2 (COX-2) expression.

Main Results:

  • Co-treatment of pKr-2 with IL-13/IL-4 induced microglia cell death.
  • Increased ROS production and COX-2 expression were observed.
  • Inhibition of NADPH oxidase and antioxidants partially reduced ROS and cell death.
  • COX-2 inhibition reversed microglia cell death.

Conclusions:

  • Oxidative stress and COX-2 activation via NADPH oxidase contribute to IL-13/IL-4 induced microglia cell death.
  • pKr-2 in combination with IL-13/IL-4 triggers a pathway leading to microglia apoptosis.
Keywords:
COX-2Interleukin-13Interleukin-4MicrogliaNADPH oxidaseProthrombin kringle-2

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