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PIDD Mediates Radiation-Induced Microglia Activation.

Nong Yang1, Xican Gao2, Xiaofei Qu2

  • 1a   Lung Cancer and Gastroenterology Department, Hunan Cancer Hospital, Affiliated Tumor Hospital of Xiangya Medical School of Central South University, Changsha, 410006, China; and.

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Silencing p53-induced protein with a death domain (PIDD) inhibits radiation-induced microglial activation and pro-inflammatory cytokine release, offering a potential new strategy for treating radiation-induced brain injury (RIBI).

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Area of Science:

  • Neuroscience
  • Radiation Oncology
  • Molecular Biology

Background:

  • Radiation-induced brain injury (RIBI) is a common consequence of cranial radiation therapy (CRT).
  • Microglial activation and pro-inflammatory cytokine release are implicated in RIBI pathogenesis and hippocampal neurogenesis inhibition.

Purpose of the Study:

  • To investigate the role of p53-induced protein with a death domain (PIDD) in radiation-induced microglial activation.
  • To explore PIDD's involvement in the PIDD-C/NF-κβ transcription pathway and radiation-induced apoptosis.

Main Methods:

  • BV-2 microglial cells were transfected with control or PIDD-targeted antisense oligonucleotides.
  • Cells were subjected to sham or 16 Gy irradiation.
  • Microglial activation and pro-inflammatory cytokine expression were assessed using RT-PCR, Western blotting, immunofluorescence, and flow cytometry.

Main Results:

  • Silencing PIDD expression significantly inhibited radiation-induced microglial activation.
  • PIDD downregulation reduced the expression of pro-inflammatory cytokines.
  • PIDD was identified as a key regulator of the PIDD-C/NF-κβ pathway and a switcher between this pathway and radiation-induced apoptosis.

Conclusions:

  • PIDD plays a critical role in radiation-induced microglial activation and subsequent inflammatory responses.
  • Targeting PIDD offers a potential novel therapeutic strategy for mitigating radiation-induced brain injury.
  • This study provides insights into combination treatments for RIBI by modulating PIDD-mediated pathways.