RNA-seq Analysis of Spinal Cord Tissues after Brachial Plexus Root Avulsion in Mice

Abstract

Background Brachial plexus root avulsion (BPRA) can cause motor neuron death, nerve degeneration and upper limb motor dysfunction. The molecular mechanisms of motor neuron death and nerve degeneration are largely unknown and there are no effective therapies to increase the functional recovery after BRPA.

Aim: To detect the early pathway changes in spinal cord tissues after brachial plexus root avulsion.

Methods A mouse brachial plexus avulsion and re-implantation model was constructed, and the C5-C7 segments of the spinal cords were dissected three days after the surgery. We used RNA-seq to identify the expression changes of genes and gene networks in spinal cord tissues.

Results A total of 2253 differentially expressed genes were found significantly changed with 1852 upregulated and 401 downregulated at 3 days after BPRA. Gene ontology (GO) enrichment analysis showed that differentially expressed genes were most enriched in immune system process, regulation of immune system process, defense response, plasma membrane part, extracellular region part, cell surface, protein binding, receptor binding, glycosaminoglycan binding. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that the most enriched pathways included osteoclast differentiation, NF-kappa B, cytokine-cytokine receptor interaction, TNF, hematopoietic cell lineage, complement and coagulation cascades, PI3K-Akt, ECM-receptor interaction, NOD-like receptor, Toll-like receptor signaling pathway.

Conclusions This study systematically identified the critical genes and signaling pathways in BPRA pathology. These results expand our understanding of the complex molecular mechanisms involved in BPRA and provide a foundation for future research of spinal cord tissue injury and repair.