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Blocking TRAIL-DR5 signaling with soluble DR5 reduces delayed neuronal damage after transient global cerebral

Min Cui1, Limei Wang, Xiaohong Liang

  • 1Department of Physiology, Shandong University School of Medicine, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, P.R. China. cuimin@sdu.edu.cn <cuimin@sdu.edu.cn>

Neurobiology of Disease
|April 3, 2010
PubMed

Insights

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) exacerbates brain damage after ischemic stroke. Inhibiting TRAIL function offers a potential neuroprotective strategy for treating stroke by reducing neuronal death.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Delayed selective neuronal death following global cerebral ischemia is not fully understood.
  • The role of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in cerebral ischemia pathogenesis requires further investigation.

Purpose of the Study:

  • To elucidate the role of TRAIL in the mechanisms of delayed neuronal death after global cerebral ischemia.
  • To evaluate the potential of inhibiting TRAIL as a neuroprotective strategy for ischemic stroke.

Main Methods:

  • Transient global brain ischemia was induced in C57BL/6j mice.
  • Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry were used to assess TRAIL and DR5 expression.
  • Dual immunofluorescence analysis identified cell-specific expression patterns.
  • Treatment with soluble DR5 was administered to evaluate its effect on ischemic cell death.

Main Results:

  • TRAIL and DR5 expression were upregulated post-ischemia-reperfusion.
  • TRAIL was predominantly expressed in astrocytes and activated microglia/macrophages, while DR5 was mainly in neurons.
  • Neuronal apoptosis correlated with the distribution of TRAIL and DR5 expression.
  • Soluble DR5 treatment reduced ischemic cell death by blocking TRAIL-DR5 interaction.

Conclusions:

  • TRAIL plays a detrimental role in delayed neuronal damage after global cerebral ischemia.
  • Inhibition of TRAIL function presents a promising neuroprotective therapeutic strategy for ischemic stroke.

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