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Updated: Feb 14, 2026
Measuring Calpain Activity in Fixed and Living Cells by Flow Cytometry
Published on: July 8, 2010
MiR-137-3p rescue motoneuron death by targeting calpain-2
Ying Tang1, Rao Fu1, Ze-Min Ling1
1Department of Anatomy, Zhongshan School of Medicine, Sun Yat-sen University, No. 74 Zhongshan Road 2, Guangzhou, 510080, PR China; Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, No. 74 Zhongshan Road 2, Guangzhou, 510080, PR China.
Abstract:
Brachial plexus root avulsion (BPRA) is a type of injury that leads to motor function loss as a result of motoneurons (MNs) degeneration. Here we identified that the reduced expression of rat miR-137-3p in the ventral horn of spinal cord was associated with MNs death. However, the pathophysiological role of miR-137-3p in root avulsion remains poorly understood. We demonstrated that the calcium-activated neutral protease-2 (calpain-2) was a direct target gene of miR-137-3p with miR-137-3p binding to the 3'-untranslated region of calpain-2. Silencing of calpain-2 suppressed the expression of neuronal nitric oxide synthase (nNOS), a primary source of nitric oxide (NO). After avulsion 2 weeks, up-regulation of miR-137-3p in the spinal cord reduced calpain-2 levels and nNOS expression inside spinal MNs, resulting in an amelioration of the MNs death. These events provide new insight into the mechanism by which upregulation of miR-137-3p can impair MN survival in the BPRA.
Insights
Upregulating miR-137-3p in spinal cord injury (brachial plexus root avulsion) reduces motoneuron death by targeting calpain-2 and neuronal nitric oxide synthase. This finding offers new therapeutic insights for brachial plexus root avulsion.
Area of Science:
- Neuroscience
- Molecular Biology
- Regenerative Medicine
Background:
- Brachial plexus root avulsion (BPRA) causes motor neuron (MN) degeneration and loss of function.
- Reduced miR-137-3p expression in the spinal cord ventral horn is linked to MN death after BPRA.
- The precise role of miR-137-3p in BPRA pathophysiology is not fully understood.
Purpose of the Study:
- To investigate the role of miR-137-3p in motoneuron survival following brachial plexus root avulsion.
- To identify the molecular targets and pathways regulated by miR-137-3p in the context of BPRA.
Main Methods:
- Investigated the interaction between miR-137-3p and calpain-2 using molecular biology techniques.
- Assessed the effects of miR-137-3p modulation on calpain-2 and neuronal nitric oxide synthase (nNOS) expression in spinal cord tissues.
- Evaluated the impact of miR-137-3p upregulation on motoneuron survival after experimental brachial plexus root avulsion.
Main Results:
- Calpain-2 was identified as a direct target gene of miR-137-3p, with binding occurring in the 3'-untranslated region.
- Silencing calpain-2 led to decreased expression of nNOS.
- Upregulation of miR-137-3p in the spinal cord two weeks post-avulsion reduced calpain-2 and nNOS levels in spinal motoneurons, mitigating motoneuron death.
Conclusions:
- miR-137-3p directly targets calpain-2, influencing nNOS expression and nitric oxide production.
- Upregulating miR-137-3p in the spinal cord shows potential for protecting motoneurons against degeneration in brachial plexus root avulsion.
- These findings elucidate a novel mechanism contributing to motoneuron survival in BPRA and suggest therapeutic avenues.
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