Investigate the role of MLKL in regulating TNF-induced endothelial cell inflammatory response

Purpose: Analyze the potential signaling pathways regulated by MLKL under TNF-induced endothelial cell inflammatory response Methods: HUVECs were allowed to grow to confluency and were starved with basal medium containing 0.5% FBS for 6h. Then treat HUVECs with vehicle, NSA, TNF-alpha, TNF-alpha+NSA for 6h and extract RNA. Results: NSA reduces the mRNA level of TNF-induced inflammation-related genes and most of these genes are downstream of NF-kappa B signaling pathway. Overall design: mRNA profiles of HUVECs treated with vehicle, NSA, TNF-alpha, TNF-alpha+NSA were generated by sequencing.