Effect of vasostatin-2 treatment on gene expression in mouse femoral arteries following wire injury

Neointimal hyperplasia is a major pathological process underlying restenosis following vascular injury. Vasostatin-2, a bioactive peptide derived from chromogranin A, has been implicated in vascular protection, but its mechanism remains unclear. To investigate the molecular basis through which vasostatin-2 modulates vascular remodeling, we performed transcriptomic profiling using RNA sequencing in a mouse model of femoral artery wire injury. Mice underwent wire-induced endothelial denudation of the femoral artery and immediately received perivascular treatment with either vasostatin-2 or saline. At 3 days post-injury, the injured femoral arteries were harvested for RNA-seq analysis to examine the impact of vasostatin-2 treatment on gene expression changes associated with vascular injury and neointima formation. This dataset provides insight into the transcriptional programs regulated by vasostatin-2 during the early phase of vascular injury and may reveal therapeutic targets for preventing restenosis. RNA sequencing was performed on mouse femoral arteries 3 days post-wire injury, following perivascular treatment with either vasostatin-2 or saline, with three biological replicates per group, to examine gene expression changes associated with vascular injury and neointima formation.