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Updated: Jun 28, 2025
Neural Stem Cell Transplantation in Experimental Contusive Model of Spinal Cord Injury
Published on: December 17, 2014
TP53INP2 knockdown inhibits inflammatory response and apoptosis after spinal cord injury
Penghao Sun1, Jinchuan Chen1, Rujie Qin1
1Department of Spine Surgery, The First People's Hospital of Lianyungang, Lianyungang, China.
Background:
Spinal cord injury (SCI) is a traumatic neurological disorder with limited therapeutic options. Tumor protein p53-inducible nuclear protein 2 (TP53INP2) is involved in the occurrence and development of various diseases, and it may play a role during SCI via affecting inflammation and neuronal apoptosis. This study investigated the associated roles and mechanisms of TP53INP2 in SCI.
Methods:
Mouse and lipopolysaccharide (LPS)-induced SCI BV-2 cell models were constructed to explore the role of TP53INP2 in SCI and the associated mechanisms. Histopathological evaluation of spinal cord tissue was detected by hematoxylin and eosin staining. The Basso, Beattie, and Bresnahan score was used to measure the motor function of the mice, while the spinal cord water content was used to assess spinal cord edema. The expression of TP53INP2 was measured using RT-qPCR. In addition, inflammatory factors in the spinal cord tissue of SCI mice and LPS-treated BV-2 cells were measured using enzyme-linked immunosorbent assay. Apoptosis and related protein expression levels were detected by flow cytometry and western blot analysis, respectively.
Results:
TP53INP2 levels increased in SCI mice and LPS-treated BV-2 cells. The results of in vivo and in vitro experiments showed that TP53INP2 knockdown inhibited the inflammatory response and neuronal apoptosis in mouse spinal cord tissue or LPS-induced BV-2 cells.
Conclusions:
After spinal cord injury, TP53INP2 was upregulated, and TP53INP2 knockdown inhibited the inflammatory response and apoptosis.
Insights
Tumor protein p53-inducible nuclear protein 2 (TP53INP2) levels rise after spinal cord injury (SCI). Reducing TP53INP2 expression mitigates inflammation and neuronal cell death in SCI models.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Spinal cord injury (SCI) is a severe neurological condition with limited treatment strategies.
- Tumor protein p53-inducible nuclear protein 2 (TP53INP2) is implicated in various disease processes.
- TP53INP2 may influence SCI outcomes by modulating inflammation and neuronal apoptosis.
Purpose of the Study:
- To investigate the role and underlying mechanisms of TP53INP2 in spinal cord injury.
- To determine if TP53INP2 expression is altered following SCI.
- To assess the therapeutic potential of targeting TP53INP2 in SCI.
Main Methods:
- Established mouse models of SCI and lipopolysaccharide (LPS)-induced BV-2 cell injury.
- Assessed spinal cord pathology, motor function (Basso, Beattie, and Bresnahan score), and edema.
- Quantified TP53INP2 expression (RT-qPCR), inflammatory factors (ELISA), and apoptosis (flow cytometry, Western blot).
Main Results:
- TP53INP2 expression was significantly upregulated in both SCI mice and LPS-treated BV-2 cells.
- Knockdown of TP53INP2 effectively reduced inflammatory responses in SCI and LPS-induced models.
- TP53INP2 inhibition also decreased neuronal apoptosis in the studied models.
Conclusions:
- TP53INP2 is upregulated following spinal cord injury.
- Targeting TP53INP2 demonstrates a protective effect by inhibiting inflammation and apoptosis.
- TP53INP2 represents a potential therapeutic target for managing spinal cord injury.
