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Blocking TRAIL-DR5 signaling with soluble DR5 alleviates acute kidney injury in a severely burned mouse model

Xiangfeng Leng1, Qiu Zhang2, Zhenyu Chen1

  • 1Department of Plastic Surgery, The Affiliated Hospital of Medical College Qingdao University Qingdao 266003, Shandong, China.

International Journal of Clinical and Experimental Pathology
|July 18, 2014
PubMed

Insights

Burn injury significantly increases apoptosis in the kidneys, mediated by tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and Death receptor 5 (DR5). Blocking TRAIL-DR5 signaling protects against burn-induced acute kidney injury (AKI).

Area of Science:

  • Nephrology
  • Burn Injury Research
  • Molecular Biology

Background:

  • Acute kidney injury (AKI) is a critical complication in severe burn patients, associated with high mortality.
  • Apoptosis is implicated in AKI pathogenesis, but the specific mechanisms in burn-induced AKI remain unclear.

Purpose of the Study:

  • To investigate the role of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and its receptor, Death receptor 5 (DR5), in the development of AKI following burn injury.

Main Methods:

  • Male C57BL/6 mice underwent full-thickness scald burn.
  • Kidney apoptosis, TRAIL, and DR5 expression were assessed 24 hours post-burn.
  • The effect of soluble DR5 treatment on burn-induced kidney injury was evaluated.

Main Results:

  • Burn injury significantly upregulated apoptosis in mouse kidneys.
  • Expression of TRAIL and DR5 was markedly increased in the kidneys after burn injury.
  • Administration of soluble DR5 reduced apoptotic cell death and mitigated kidney injury by inhibiting TRAIL-DR5 interaction.

Conclusions:

  • TRAIL-DR5 signaling plays a detrimental role in the pathogenesis of burn-induced AKI.
  • Inhibiting TRAIL function in the kidney presents a potential therapeutic strategy for managing AKI in burn patients.
Keywords:
DR5TRAILacute kidney injuryapoptosisburn

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