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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Reactive oxygen species in TNFalpha-induced signaling and cell death

Michael J Morgan1, Zheng-Gang Liu

  • 1Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA.

Molecules and Cells
|July 24, 2010
PubMed

Insights

Tumor necrosis factor-alpha (TNFalpha) triggers cell death pathways and reactive oxygen species (ROS) generation. ROS can modulate these pathways, influencing apoptosis and NF-kappaB signaling.

Area of Science:

  • Cellular signaling
  • Molecular biology
  • Immunology

Background:

  • Tumor necrosis factor-alpha (TNFalpha) is a key cytokine regulating cellular processes.
  • TNFalpha initiates multiple downstream signaling cascades, including NF-kappaB and MAP kinase pathways.
  • TNFalpha is implicated in both apoptosis and necrosis.

Purpose of the Study:

  • To elucidate the intricate relationship between TNFalpha, reactive oxygen species (ROS), and cell death signaling.
  • To explore the dual role of ROS in modulating TNFalpha-induced signaling pathways.
  • To highlight the specific impact of ROS on JNK and NF-kappaB activation.

Main Methods:

  • Review and synthesis of existing literature on TNFalpha signaling and ROS.
  • Analysis of mechanisms by which TNFalpha induces ROS production.
  • Examination of the modulatory effects of ROS on key signaling molecules like JNK and NF-kappaB.

Main Results:

  • TNFalpha induces ROS generation via NADPH oxidase and mitochondrial pathways.
  • ROS potentiate sustained JNK activation, promoting apoptosis and necrotic cell death.
  • ROS exhibit complex regulatory roles, potentially inhibiting or stimulating NF-kappaB signaling.

Conclusions:

  • ROS are critical mediators in TNFalpha-induced cell fate.
  • The interplay between TNFalpha and ROS significantly influences apoptotic and necrotic outcomes.
  • Understanding these interactions is crucial for targeting inflammatory and cell death processes.

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