Paxillin mediates endothelial cell migration and angiogenesis following spinal cord injury: a transcriptomic and functional analysis.

Spinal cord injury (SCI) is a destructive neurological condition that leads to significant functional deficits in the affected individual. To map the altered pathways within the lesion epicentre and the surrounding rostrocaudal segments, we performed RNA-sequencing on injured spinal cord tissue. Samples were collected from three regions-rostral, epicentre, and caudal-at Days 1, 14, and 28 post-injury to systematically profile the transcriptomic changes and identify pathways associated with angiogenesis following SCI. Gene set enrichment analysis revealed enriched pathways, including hepatocyte growth factor (HGF) receptor and alpha 6 beta 4 integrin signalling, indicating an active angiogenic response. The involvement of HGF receptor signalling was further validated by quantitative polymerase chain reaction (qPCR), confirming its role in pathological remodelling after SCI. Subsequently, we identified paxillin (Pxn) as a candidate gene that promotes endothelial cell migration via HGF receptor signalling. Immunohistochemistry demonstrated the role of Pxn in mediating endothelial cell migration and proliferation post-SCI. In summary, our findings indicate that Pxn is a key mediator of endothelial cell proliferation and migration in response to angiogenic factors, such as HGF, following SCI. However, further mechanistic studies are required to fully establish the role of Pxn in endothelial cell migration and proliferation after SCI.