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Published on: August 15, 2012
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.
Abstract:
Radiation-induced brain injury (RIBI) is the most common adverse effect that occurs after cranial radiation therapy (CRT). We have previously reported that CRT-induced release of pro-inflammatory cytokines in brain tissues and inhibition of neurogenesis in the hippocampus might be caused by microglial activation and may play an important role in RIBI. In this study we examined the role of p53-induced protein with a death domain (PIDD) in radiation-induced activation of BV-2 cells. BV-2 cells were transfected with antisense oligonucleotide control mRNA or antisense oligonucleotide-targeted PIDD mRNA and were sham or 16 Gy irradiated. The state of microglia and expression of pro-inflammatory cytokines were detected using real-time polymerase chain reaction, Western blotting, immunofluorescence and flow cytometry. Findings from this study suggest that silencing PIDD expression could inhibit microglial activation by downregulating the PIDD-C/NF-κβ transcription pathway. PIDD acts as a critical switcher between the NF-κβ transcription pathway and radiation-induced apoptosis. Given these findings, this study offers a potential novel approach to further combination treatment of RIBI.
Insights
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).
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.
