Transcriptomic analysis of human coronary artery endothelial cells stimulated with TNF-alpha in the presence and absence of ACSL3 siRNA

TNF-alpha has a number of pro-atherogenic effects in macrovascular endothelial cells, including induction of leukocyte adhesion molecules and chemokines. We investigated the role of acyl-CoA synthetase 3 (ACSL3) in the response of cultured human macrovascular endothelial cells to TNF-alpha. TNF-alpha induced ACSL3 both in human umbilical vein endothelial cells (HUVECs) and in human coronary artery endothelial cells (HCAECs). RNA sequencing demonstrated that knockdown of ACSL3 had no marked effects on the TNF-alpha transcriptome in HCAECs. Instead, ACSL3 was required for TNF-alpha-induced lipid droplet formation from fatty acids. Samples analyzed in triplicates from one donor, 4 different conditions (basal+control siRNA, TNF-alpha+control siRNA, basal+ACSL3 siRNA, TNF-alpha+ACSL3 siRNA)