Transcriptomic analysis of α-synuclein knockdown after T3 spinal cord injury in rats.

摘要: Endogenous α-synuclein (α-Syn) is involved in many pathophysiological processes the secondary injury stage after acute spinal cord (SCI), and mechanism governing these functions has not been thoroughly elucidated to date. This research aims characterize effect of α-Syn knockdown on transcriptional levels SCI determine mechanisms underlying activity based RNA-seq. The establishment a rat model lentiviral vector-mediated Sprague-Dawley rats with T3 contusion (LV_SCI group). results RNA-seq analysis showed that there were 337 differentially expressed genes (DEGs) between group LV_SCI group, 153 DEGs specific (SCI vs LV_SCI) CON) comparisons. top 20 biological transition terms identified by Gene ontology (GO) analysis. Kyoto Genomic Encyclopedia (KEGG) significantly upregulated cholinergic synaptic & nicotine addiction neuroactive ligand receptor interaction signaling pathway. Enriched chord analyzes key genes. Further cluster analysis, gene protein network RT-qPCR Chrm2 Chrnb2 together both pathways. proliferation muscarinic subtype 2 (Chrm2) nicotinic β2 (Chrnb2), neurogenesis elevated site immunofluorescence. subcellular localization, enhanced expression at cell membrane. Knockdown enhance motor function promote probably through enhancing pathways neuroreceptor interactions. study only further clarifies understanding but also helps guide treatment strategy for SCI.