Up-regulation of heat shock protein 27 inhibits apoptosis in lumbosacral nerve root avulsion-induced neurons

Zhi-Bin Zhou,Jun Ma,Gao-Xiang Huang,Yan Cao,Qi-Jun Yuan,Jia-Jia Lu,Lei Zhu

doi:10.1038/s41598-019-48003-9

Abstract

Lumbosacral nerve root avulsion leads to widespread death of neurons in the anterior horn area of the injured spinal cord, which results in dysfunction in the lower extremities. Heat shock protein 27 (Hsp27) has been found to play cytoprotective roles under adverse conditions. However, the role of Hsp27 in neurons after lumbosacral nerve root avulsion is unknown. The aim of the present study was to investigate the effects and mechanism of action of Hsp27 on neurons after lumbosacral nerve root avulsion. It was found that Hsp27 expression was elevated in the anterior horn area of the injured spinal cord and the up-regulation of Hsp27 protected neurons against apoptosis after lumbosacral nerve root avulsion. In addition, Hsp27 plays an anti-apoptotic role by suppressing oxidative stress reactions. These findings indicated that Hsp27 may play a key role in resistance to lumbosacral nerve root avulsion-induced neuron apoptosis and may prove to be a potential strategy for improving prognosis after lumbosacral nerve root avulsion.

Highlights

Lumbosacral nerve root avulsion causes the physical disconnection of nerve roots from the spinal cord, which leads to widespread neuron death in the anterior horn area of the injured spinal cord[1]
The immunofluorescent staining assay showed that the level of Heat shock protein (Hsp)[27] protein was elevated in neurons located in the anterior horn of the avulsion side of the spinal cord, at 3 d after surgery compared with the sham-operation group (Fig. 1c)
We found that lumbosacral nerve root avulsion increased the number of apoptotic neurons of the anterior horn of the spinal cord in the scramble short hairpin RNA (shRNA)-transfected group and the apoptosis index increased to 49% after lumbosacral nerve root avulsion (p < 0.01) (Fig. 3b,c)

Summary

Introduction

Lumbosacral nerve root avulsion causes the physical disconnection of nerve roots from the spinal cord, which leads to widespread neuron death in the anterior horn area of the injured spinal cord[1]. This severe neuron death results in devastating motor dysfunction, neuropathic pain, and numbness in the lower extremities[2,3,4,5]. The aim of our study was to reveal whether the expression of Hsp[27] was upregulated after lumbosacral nerve root avulsion and oxygen-glucose deprivation (OGD). The findings suggested that Hsp[27] inhibited apoptosis and may prove to be a strategy for improving prognosis after lumbosacral nerve root avulsion

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Conclusion