RNA-seq Reveals Paxillin as a Key Facilitator of Endothelial Cell Migration and Angiogenesis after Spinal Cord Injury

Spinal cord injury (SCI) is a catastrophic condition resulting in significant neurological deficits. To map the altered pathways within the lesion epicenter and the surrounding rostro-caudal segments, we employed RNA-seq on injured spinal cord tissue. We sequenced samples from three level (rostral, epicenter, and caudal) at days 1, 14, and 28 post-injury to systematically define the transcriptomics profile, aiming to identify pathways related to angiogenesis after SCI. Gene set enrichment analysis (GSEA) revealed enriched pathways, including hepatocyte growth factor (HGF) receptor signalling and alpha-6 beta-4 signaling pathway, suggesting an active angiogenic signature. Furthermore, the participating genes in HGF receptor signaling were validated by qPCR analysis, demonstrating that HGF receptor signaling is involved in the pathological remodeling following SCI. Subsequently, we investigated paxillin as a candidate gene promoting endothelial cell migration through HGF receptor signaling. Immunohistochemistry data suggest paxillin’s role in mediating the endothelial cell migration and proliferation post-SCI. In summary, our findings indicate that paxillin is a key mediator of endothelial cell proliferation and migration in response to angiogenic factors like HGF following SCI. However, extensive mechanistic studies are required to fully establish paxillin’s role in endothelial cell migration and proliferation after SCI. Transcriptomics alterations were validated spatiotemporally in contusion model of spina cord injury at DPI-1, DPI-14, and DPI-28.