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Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury
Published on: May 27, 2022
PDCD1 Signaling in Microglia Can Reduce Neuroinflammation and Apoptosis Induced by Traumatic Brain Injury by
Jinjie Tian1, Yao Wang1, Jing Zhao2
1Department of Neurosurgery, Affiliated Nantong Clinical College of Nantong University; Nantong Clinical Medical College of Kangda College of Nanjing Medical University; Nantong First Peoples Hospital, Southeast University, Nantong, 226001, China.
Molecular Neurobiology
|August 7, 2026
Summary
Programmed cell death protein-1 (PDCD1) mitigates neuroinflammation and nerve cell death after traumatic brain injury (TBI). This signaling pathway, primarily in microglia and neurons, improves cognitive and motor functions post-TBI.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Traumatic brain injury (TBI) often leads to neuroinflammation and neuronal cell death, negatively impacting patient prognosis.
- Programmed cell death protein-1 (PDCD1) signaling is implicated in TBI's pathological processes.
Purpose of the Study:
- To investigate the role of PDCD1 signaling in TBI-induced neuroinflammation and neuronal cell death.
- To assess PDCD1's impact on cognitive, memory, and motor function recovery after TBI.
- To elucidate the underlying molecular mechanisms of PDCD1's action.
Main Methods:
- Utilized a controlled cortical impact (CCI) murine model for in vivo TBI.
- Established an in vitro microglial inflammation model using BV-2 cells stimulated with lipopolysaccharide (LPS).
- Analyzed PDCD1 expression, knockdown, and overexpression effects on inflammatory markers (IL-1β, iNOS, Bax, Bcl-2) and signaling pathways (PI3K/Akt).
Main Results:
- TBI significantly increased PDCD1 expression, predominantly in microglia and neurons.
- PDCD1 knockdown exacerbated neuroinflammation and cell death, while PDCD1 overexpression showed protective effects.
- PDCD1 activation was linked to the PI3K/Akt pathway, suggesting its involvement in mitigating TBI-induced damage.
Conclusions:
- PDCD1 plays a crucial role in mitigating neuroinflammation and neuronal cell death following TBI.
- PDCD1 signaling, partly through the PI3K/Akt pathway, contributes to functional recovery after TBI.
- Targeting PDCD1 may offer a therapeutic strategy for managing TBI outcomes.