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Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue
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Rapid mitochondrial dysfunction mediates TNF-alpha-induced neurotoxicity.

Danielle N Doll1, Stephanie L Rellick, Taura L Barr

  • 1Neurobiology and Anatomy, West Virginia University, Morgantown, West Virginia, USA; Center for Neuroscience, Morgantown, WV, USA; Center for Basic and Translational Stroke Research, Morgantown, WV, USA.

Journal of Neurochemistry
|December 11, 2014
PubMed
Summary

Tumor necrosis factor alpha (TNF-α) rapidly impairs brain cell mitochondrial function and viability at post-stroke concentrations. This neuroinflammation mechanism, mediated by TNF-R1, offers potential neuroprotection targets.

Keywords:
TNF-alphacytokinesinflammationmitochondrianeuro-toxicitystroke

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Tumor necrosis factor alpha (TNF-α) exacerbates ischemic brain injury, but its precise mechanism remains unclear.
  • Previous research used non-pathophysiologically relevant high doses and long exposure times for TNF-α.
  • Understanding rapid TNF-α effects at relevant concentrations is crucial for ischemic brain injury.

Purpose of the Study:

  • To characterize the rapid effects of pathophysiologically relevant TNF-α concentrations on neuronal mitochondrial function and viability.
  • To elucidate the specific mechanism by which TNF-α induces neurotoxicity.
  • To identify potential therapeutic targets for neuroprotection against TNF-α-mediated damage.

Main Methods:

  • Assessed basal, ATP, and maximal respiration in neurons exposed to low doses of TNF-α.
  • Utilized HT-22 cell line and primary neurons for experiments.
  • Investigated the role of TNF-R1 and TNF-R2 receptors using antibody pre-treatment.
  • Measured caspase 8 activity, mitochondrial membrane potential, and cytochrome c release.

Main Results:

  • A significant reduction in mitochondrial function was observed as early as 1.5 hours after TNF-α exposure.
  • Cell viability decreased in HT-22 cells and primary neurons following TNF-α treatment.
  • Neurotoxic effects were ameliorated by TNF-R1 antibody pre-treatment, implicating TNF-R1 signaling.
  • Increased caspase 8 activity, decreased mitochondrial membrane potential, and cytochrome c release were observed.

Conclusions:

  • Acute exposure to pathophysiologically relevant TNF-α concentrations causes rapid neurotoxicity.
  • TNF-α impairs mitochondrial function, leading to nerve cell loss via TNF-R1 signaling.
  • This study highlights the immune system's rapid adverse effects on brain function and suggests TNF-α signaling as a neuroprotection target.