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Mitochondria released by cells undergoing TNF-α-induced necroptosis act as danger signals

A Maeda1, B Fadeel1

  • 1Division of Molecular Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Cell Death & Disease
|July 4, 2014
PubMed

Insights

Dying cells release intact mitochondria during programmed necrosis. These released mitochondria act as danger signals, influencing immune cell responses and maturation.

Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Biology

Background:

  • Necrosis releases damage-associated molecular patterns (DAMPs), potentially causing inflammation.
  • The release and function of organelles from dying cells remain largely uncharacterized.

Purpose of the Study:

  • To investigate the release of organelles during programmed necrosis.
  • To determine the characteristics and functional consequences of mitochondria released from necroptotic cells.

Main Methods:

  • Induction of necroptosis using tumor necrosis factor-α (TNF-α) and receptor-interacting protein 1 (RIP1) inhibition.
  • Purification and analysis of released mitochondria.
  • Assessment of mitochondrial integrity via mitochondrial DNA (mtDNA) release.
  • Pharmacological inhibition of dynamin-related protein 1 (Drp1).
  • Co-culture experiments with primary human macrophages and dendritic cells.

Main Results:

  • Mitochondria are released from cells undergoing TNF-α-induced, RIP1-dependent necroptosis.
  • Released mitochondria are intact and do not significantly release mtDNA.
  • Inhibition of mitochondrial fission (Drp1) did not prevent necroptosis or mitochondrial release.
  • Engulfment of necroptotic mitochondria by immune cells modulated cytokine secretion and induced dendritic cell maturation.

Conclusions:

  • Intact mitochondria are released from necroptotic cells.
  • Released mitochondria function as danger signals, impacting immune cell behavior.
  • This identifies a novel mechanism of intercellular communication in cell death pathways.

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