Downregulation of Engulfment and cell motility 1 (Elmo1) induces quiescence and resistance to poly(I:C)-induced apoptosis in endothelial cells
Engulfment and Cell Motility 1 (ELMO1) facilitates activation of Ras-related C3 botulinum toxin substrate 1 (RAC1) through interaction with Dedicator of Cytokinesis (DOCK), a family of guanine nucleotide exchange factors (GEF). ELMO1 plays an important role in acute and chronic inflammation by enhancing immune cell migration, phagocytosis of pathogens and dead cells, and production of reactive oxygen species. Endothelial cells, an integral component of inflammatory responses, also express high levels of ELMO1, although the role of ELMO1 in inflammatory endothelial cells is unclear. We demonstrate that knockdown of ELMO1 in EA.hy926 human umbilical vein endothelial cells (HUVECs) leads to cell quiescence, while protects the cells from Toll-like receptor 3 (TLR3)-induced apoptosis and restores inflammatory responses. Overall design: RNA-seq profiling of EA.hy926 human umbilical vein endothelial cells treated with transfection reagents-only (Mock), cells transfected with non-targeting siRNA (siNT), and those with ELMO1-targeting siRNA (siELMO1), before (0 h) and after (24 h) the stimulation with poly(I:C)