Disfunction of arachidonic acid metabolism in vascular smooth muscle cells contributes to restenosis. Disfunction of arachidonic acid metabolism in vascular smooth muscle cells contributes to restenosis

We applied the transcriptome profiling (RNA-seq) for high-throughput profiling of genes changes in the phenotypic switch of VSMCs. Rat primary VSMCs were divided into 3 groups, control, PDGF-BB, PDGF-BB+PTUPB,and mRNA sequence were performed. We found that Cell cycle related genes and cellular senescence related genes were significantly upregulated by PDGF-BB and significantly reversed by PTUPB. Subsequently, we deleted PTTG1 as a key gene for PTUPB to reverse phenotypic switching in VSMCs. Our study provided the transcription changes by RNA-seq in VSMC phenotypic switch, and found that PTUPB played a crucial role in correcting the dysregulation of sEH/COX-2 derived ARA metabolism in VSMC phenotypic switch Overall design: In order to understand how PTUPB reverses the phenotypic transition of PDGF-BB-induced VSMCs, we divided rat primary VSMCs into control, PDGF-BB (20 ng/mL) stimulation for 24 h, and PTUPB pretreatment (0.5 μM,2h) followed by PDGF-BB stimulation for 24 h. We performed NGS RNAseq on these groups.Each group included three VSMCs.