Serine-threonine protein kinase activation may be an effective target for reducing neuronal apoptosis after spinal cord injury

Neural Regeneration Research, 2015 · DOI: 10.4103/1673-5374.170313 · Published: November 1, 2015

Simple Explanation

This study investigates the signaling pathways involved in nerve cell death (apoptosis) after spinal cord injury caused by reduced blood flow (ischemia). The focus is on three specific pathways: ERK, Akt, and JNK. The researchers created a rat model of spinal cord injury and observed changes in these pathways over time. They found that activating the Akt pathway might help protect nerve cells from dying after injury. These findings suggest that targeting the Akt pathway could be a way to develop new treatments for spinal cord injuries, aiming to reduce nerve cell death and improve recovery.

Study Duration

72 hours

Participants

90 male Sprague-Dawley rats

Evidence Level

Not specified

Key Findings

1
The expression of phosphorylated Akt (p-Akt) and phosphorylated ERK (p-ERK) increased immediately after reperfusion, peaked at 4 hours (p-Akt) or 2 hours (p-ERK), decreased at 12 hours, and then increased at 24 hours.
2
Phosphorylated JNK expression reduced after reperfusion, increased at 12 hours to near normal levels, and then showed a downward trend at 24 hours.
3
Pearson linear correlation analysis also demonstrated that the number of apoptotic cells negatively correlated with p-Akt expression.

Research Summary

The study investigates the effects of apoptosis-related signal transduction pathways following ischemic spinal cord injury, including extracellular signal-regulated kinase (ERK), serine-threonine protein kinase (Akt) and c-Jun N-terminal kinase (JNK) signaling pathways. The number of apoptotic neurons was highest 48 hours post injury. Activation of Akt may be a key contributing factor in the delay of neuronal apoptosis after spinal cord ischemia, particularly at the stage of reperfusion, and thus may be a target for neuronal protection and reduction of neuronal apoptosis after spinal cord injury.

Practical Implications

Therapeutic Target Identification

Activation of Akt may serve as a therapeutic target for neuronal protection following spinal cord ischemia.

Drug Development

Drugs that enhance Akt activation could potentially reduce neuronal apoptosis and improve outcomes after spinal cord injury.

Timing of Intervention

The optimal time window for therapeutic intervention targeting Akt activation appears to be within the first 12 hours after reperfusion.

Study Limitations

1
The study was conducted on a rat model of spinal cord injury, and results may not directly translate to humans.
2
The precise mechanisms by which Akt, ERK, and JNK influence neuronal apoptosis are not fully elucidated.
3
The study only examined the spatiotemporal expression of phosphorylated Akt, JNK and ERK after permanent aortic occlusion in rats.

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