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MiR-137 attenuates spinal cord injury by modulating NEUROD4 through reducing inflammation and oxidative stress
1Department of Orthopedic, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, China. 13905239800@163.com.
Objective:
To explore the role of microRNA (miR) 137 in spinal cord injury and its mechanism.
Materials And Methods:
The model of spinal cord injury in mice was established to detect the recovery differences of grip strength in upper and lower limbs of mice. The expressions of miR-137 and neuronal differentiation 4 (NEUROD4) were detected at the same time. The inflammation level and the oxidative stress response after spinal cord injury were subsequently detected after overexpression of miR-137. Target genes of miR-137 were identified by bioinformatics. Finally, dual-luciferase reporter gene assay was used to identify the target genes of miR-137.
Results:
By establishing the model of spinal cord injury in mice, the strength of upper and lower limbs recovered after 7 days of injury in mice. The expression of miR-137 in spinal cord injury was found to decrease in a time-dependent manner by quantitative Real-time polymerase chain reaction (qRT-PCR), while the expression of NEUROD4 gradually increased. Inflammation indicators and oxidative stress level were found to be significantly higher after spinal cord injury. However, the inflammation level and oxidative stress were significantly reduced after transfection of miR-137. Finally, we predicted the target gene of miR-137 through bioinformatics website and found that NEUROD4 was a potential target gene of miR-137. Using dual luciferase reporter assays, we found that NEUROD4 bound to miR-137. After overexpression of miR-137, the expression of NEUROD4 was significantly reduced. Overexpression of NEUROD4 could promote spinal cord injury inflammation and oxidative stress. After intracellular transfection of NEUROD4 and miR-137 at the same time, the inflammation level and oxidative stress of spinal cord injury decreased significantly.
Conclusions:
These results suggested that miR-137 promoted the recovery of spinal cord injury by degrading NEUROD4 to relieve the spinal cord inflammation and the progression of oxidative stress, thus promoting the recovery of spinal cord injury.
Insights
MicroRNA 137 (miR-137) plays a crucial role in spinal cord injury recovery. Upregulating miR-137 reduces inflammation and oxidative stress by targeting NEUROD4, promoting functional recovery after injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Spinal cord injury (SCI) leads to significant functional deficits.
- MicroRNAs (miRNAs) are emerging as key regulators in neurological injury.
- The specific role of miR-137 in SCI pathogenesis and recovery remains to be fully elucidated.
Purpose of the Study:
- To investigate the role and mechanism of microRNA (miR) 137 in spinal cord injury.
- To determine if miR-137 influences inflammation and oxidative stress post-SCI.
- To identify potential therapeutic targets for SCI treatment.
Main Methods:
- Established a mouse model of spinal cord injury.
- Quantified miR-137 and NEUROD4 expression using qRT-PCR.
- Assessed inflammation and oxidative stress markers.
- Utilized bioinformatics and dual-luciferase reporter assays to identify miR-137 targets.
- Overexpressed miR-137 and NEUROD4 to evaluate their effects.
Main Results:
- miR-137 expression decreased, while NEUROD4 expression increased post-SCI.
- miR-137 overexpression significantly reduced inflammation and oxidative stress.
- NEUROD4 was identified as a direct target of miR-137.
- Overexpression of NEUROD4 exacerbated SCI-induced inflammation and oxidative stress.
Conclusions:
- miR-137 promotes spinal cord injury recovery by targeting and degrading NEUROD4.
- This mechanism alleviates spinal cord inflammation and oxidative stress.
- miR-137 represents a potential therapeutic strategy for spinal cord injury.
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