# STING deficiency promotes motor recovery in mice following brachial plexus root avulsion

## TL;DR

STING deficiency in mice improves motor recovery after brachial plexus injury by reducing nerve damage and inflammation.

## Contribution

This study reveals that STING deficiency promotes motor recovery in brachial plexus root avulsion through multiple protective mechanisms.

## Key findings

- STING deficiency increases body weight and promotes motor recovery in BPRA-affected mice.
- STING deficiency reduces motoneuron death and inhibits pyroptosis and neuroinflammation.
- STING deficiency enhances remyelination and reduces biceps brachii atrophy in BPRA mice.

## Abstract

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.

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.

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.

These combined results suggest that inhibition of STING may be a promising strategy for treating BPRA.

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.