Abstract
Introduction: Electronic-cigarette (e-cig) usage, particularly in the youth population, is a growing concern. It is known that e-cig causes endothelial dysfunction, which is a risk factor for the development of cardiovascular diseases; however, the mechanisms involved remain unclear. We hypothesized that long non-coding RNAs (lncRNAs), a novel class of non-coding RNA that has been shown to affect endothelial function, may play a role in e-cig-induced endothelial dysfunction. Methods and Results: We profiled lncRNAs that are dysregulated in human induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) from healthy individuals following 24 hours of e-cig aerosol extract treatment. Using microarray analysis, we identified that 183 lncRNAs and 132 mRNAs were upregulated while 297 lncRNAs and 413 mRNAs were downregulated. We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway analyses of the mRNAs dysregulated by e-cig exposure followed by the functional characterization of the top 5 differentially expressed (DE) lncRNAs by co-expressed protein-coding genes analysis. Interestingly, the lncRNA-mRNA association analysis revealed several mRNAs associated with metabolic disorders. Subsequently, we found that e-cig caused dysregulation of endothelial metabolism resulting in increased fatty acid oxidation activity, higher mitochondrial membrane potential, and decreased glucose uptake and glycolysis. These results suggest that e-cig-induced altered EC metabolism and increased fatty acid oxidation compensate for energy deficiency in ECs. Conclusion: Collectively, the identification of potential regulators and pathways of the interaction between lncRNAs and mRNAs in ECs treated with e-cig provides novel insights into endothelial biology and could have a significant impact on our understanding of vascular complications upon e-cig exposure.
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