Mus musculus strain:C57BL/6 Raw sequence reads

Electronic cigarettes (e-cigarettes) are a popular alternative to conventional nicotine cigarettes among both smokers and people who have never smoked cigarettes. Nicotine can induce lipolysis in adipose tissue, leading to increased serum free fatty acids (FFAs). Increased FFAs levels are one of the key elements in generating a pro-inflammatory response and lead to lipotoxicity. We investigated the effects of acipimox, an antihyperlipidemic drug that blocks lipolysis, on e-cigarette-induced cardiac dysfunction and its associated inflammatory signals and oxidative stress. C57BL/6J wild-type mice on high fat diet were exposed to saline, e-cigarettes with nicotine (2.4%), and e-cigarettes (2.4%) plus acipimox for 12 weeks. After RNA isolation from left ventricles (n=5 in each group), RNA quality was assessed with an Agilent 2100 Bioanalyzer. RNA samples exhibited clear 28S and 18S rRNA peaks and demonstrated an RNA integrity number (RIN) greater than 8. Sequencing was performed on Illumina HiSeq 3000 for a single read 50 run. Data quality check was done on Illumina SAV. Demultiplexing was performed using the Illumina Bcl2fastq2 v 2.17 program. Differentially expressed genes were identified using the edgeR program6. Genes showing altered expression with p < 0.05 and more than 1.5 fold changes were considered differentially expressed. The pathway and network analysis was performed using Ingenuity Pathway Analysis (IPA). RNA-seq transcriptomic evaluation of the heart identified genes associated with DNA damage and oxidative stress that were altered by e-cigarette exposure and normalized by acipimox. Gene Set Enrichment Analysis revealed that e-cigarette-treated mice had expression changes in both the G2/M DNA damage checkpoint and circadian pathways that were normalized by acipimox. Therefore, this RNA-seq data suggests that decreased serum FFAs has the potential to diminish detrimental, transcriptomic effects of e-cigarettes on the heart.