RNA-seq of Mouse Spinal Cord after Lateral Compression Spinal Cord Injury followed by Delayed Atorvastatin or Vehicle Treatment [Bulk RNA-seq of mice spinal cords]

This dataset supports a study investigating the effects of delayed atorvastatin treatment on gene expression and functional recovery in a chronic mouse model of spinal cord injury (SCI). Twelve-week-old female C57BL/6 mice were subjected to moderate 0.25 mm lateral compression SCI and after two weeks, were treated with atorvastatin (10 mg/kg) or a vehicle control daily for four weeks. Bulk RNA sequencing of spinal cord tissues at six weeks post-injury revealed broad alterations to gene expression due to SCI (DEGs common to both treatments and unique to each) and a smaller set of alterations due uniquely to atorvastatin treatment. Atorvastatin treatment specifically activated gene programs associated with axon guidance and fatty acid transport, which may contribute to the enhanced sensorimotor recovery. This RNA-seq dataset offers insights into the molecular underpinnings by which atorvastatin enhances sensorimotor recovery and modulates gene expression post-SCI. Overall design: To investigate the molecular effects of atorvastatin on recovery from spinal cord injury (SCI), twelve-week-old female C57BL/6 mice were divided into two groups: one receiving daily treatments of atorvastatin (10 mg/kg) dissolved in a vehicle composed of 2% dimethyl sulfoxide (DMSO), 35% polyethylene glycol (PEG) 400, 2% Tween 80, and 61% saline—and a control group receiving the vehicle alone. Treatment commenced two weeks after inducing a moderate 0.25 mm lateral compression SCI and continued for four weeks. The efficacy of atorvastatin in enhancing functional recovery was assessed before SCI and at 1, 3, and 7 days post-injury and weekly thereafter to 42 days (6 weeks) post-injury using the Basso Mouse Scale (BMS), BMS subscore, and Inclined Plane Test, with significant improvements noted by the fourth week and continuing through the final six-week post-injury assessment. At this six-week endpoint, spinal cords were harvested and subjected to bulk RNA sequencing to profile changes in gene expression. This RNA-seq run also included samples from the spinal cords of two uninjured 12-week-old female C57BL/6 mice to serve as baseline (pre-SCI, pre-treatment) controls. Analyses described in the accompanying manuscript included using DESeq2 for determining gene expression differences and applying Ingenuity Pathway Analysis and PantherGO for pathway analysis to elucidate the biological processes modulated by atorvastatin. This dataset contains raw counts of gene expression as well as gene length-normalized (transcripts per kilobase million) for each replicate for comprehensive evaluation of the transcriptomic impact of SCI and of atorvastatin on SCI recovery.