Abstract
BackgroundA sudden mechanical insult to the spinal cord is usually caused by changing pressure on the surface of the spinal cord. Most of these insults are mechanical force injuries, and their mechanism of injury to the spinal cord is largely unknown.MethodsUsing a compression-driven instrument to simulate mechanical force, we applied mechanical pressure of 0.5 MPa to rat dorsal root ganglion (DRG) neurons for 10 min to investigate cytoskeletal alterations and calpain-induced apoptosis after the mechanical force injury.ResultsThe results indicated that mechanical forces affect the structure of the cytoskeleton and cell viability, induce early apoptosis, and affect the cell cycle of DRG neurons. In addition, the calpain inhibitor PD150606 reduced cytoskeletal degradation and the rate of apoptosis after mechanical force injury.ConclusionThus, calpain may play an important role in DRG neurons in the regulation of apoptosis and cytoskeletal alterations induced by mechanical force. Moreover, cytoskeletal alterations may be substantially involved in the mechanotransduction process in DRG neurons after mechanical injury and may be induced by activated calpain. To our knowledge, this is the first report to demonstrate a relationship between cytoskeletal degradation and apoptosis in DRG neurons.
Highlights
Acute spinal cord injury (ASCI) is a major cause of persistent disability in humans [1,2]
Some studies have shown that calpain inhibitors provide neuroprotection during ASCI and indicate that calpain may have an important role in the resulting neuronal cell death [16,17]
Effects of Mechanical Force on Cell Viability We first tested the hypothesis that mechanical injury influences the cell viability of dorsal root ganglion (DRG) neurons and that calpain is involved this process
Summary
Acute spinal cord injury (ASCI) is a major cause of persistent disability in humans [1,2]. The pathological process of ASCI has two phases: the primary injury caused by a sudden mechanical force, and the secondary injury [3,4]. The delayed, secondary spinal cord injury is considered to be due to a cascade of biochemical reactions that are important in the mechanism of ASCI [5]. Calpain, a calcium-dependent cysteine protease, is involved in both the apoptotic and necrotic processes leading to neuronal cell death [14,15,16,17]. Calpain subsequently degrades many cytoskeletal and membrane proteins in the neuron [19,20,21] These cytoskeletal and membrane proteins provide architectural support for eukaryotic cells and are involved in mechanotransduction. Most of these insults are mechanical force injuries, and their mechanism of injury to the spinal cord is largely unknown
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