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STING deficiency promotes motor recovery in mice following brachial plexus root avulsion
Yu Peng1,2, Ying Zhang3, Shenhui Yang4
1Department of Neurology, Multi-Omics Research Center for Brain Disorders, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Background:
Brachial plexus root avulsion (BPRA), a well-known form of peripheral nerve injury, results in motor function loss in the affected forelimb due to motoneuron (MN) death, which may be influenced by neuroinflammation following a lesion in the spinal cord. Although synthase-stimulator of interferon genes (STING) signaling can contribute to chronic inflammation and tissue damage in a number of pathological conditions, the essential role of STING signaling in BPRA remains to be reported. Based on our previous findings that the STING mRNA level is upregulated in the anterior horn of the segment of the affected spinal cords of mice with BPRA, STING may be associated with motor recovery in BPRA.
Methods:
In the present study, STING knockout transgenic mice were used to establish a BPRA re-implantation model, which was followed by behavioral tests, histochemical staining and quantitative reverse transcription polymerase chain reaction.
Results:
The results demonstrated that STING deficiency can increase the body weight, promote motor recovery, decrease MN death, inhibit pyroptosis and neuroinflammation, increase remyelination, and reduce the atrophy of the biceps brachii in mice with BPRA.
Conclusion:
These combined results suggest that inhibition of STING may be a promising strategy for treating BPRA.
