E-MTAB-6604
RNA-Seq of human aortic endothelial cells with lysophosphatidylcholine against untreated controls
Vascular Innate immune cells, such as macrophages, elicit long-term T cell-, and B cell- immune responses, by expressing danger-associated molecular pattern (DAMP) receptors, T cell co-stimulation receptors and presenting antigens to the adaptive system through major histocompatibility complex (MHC)-II.  Here, we investigated whether human aortic endothelial cells (HAECs) could also be "transdifferentiated" into innate immune cells after treatment of lysophosphatidylcholine (LPC).  LPC specifically upregulated genes that are involved in cholesterol biosynthesis, presumably through sterol regulatory element-binding protein 2 (SREBP2).  In addition, we found that both LPC induced adhesion molecules, cytokines, and chemokines in HAECs, which are classical markers for endothelial activation.  Moreover, LPC transdifferentiated HAECs into innate immune cells including induction of potent DAMP receptors, such as CD36, T cell co-stimulation receptors and MHC-II molecules.
Vascular Innate immune cells, such as macrophages, elicit long-term T cell-, and B cell- immune responses, by expressing danger-associated molecular pattern (DAMP) receptors, T cell co-stimulation receptors and presenting antigens to the adaptive system through major histocompatibility complex (MHC)-II.  Here, we investigated whether human aortic endothelial cells (HAECs) could also be "transdifferentiated" into innate immune cells after treatment of lysophosphatidylcholine (LPC).  LPC specifically upregulated genes that are involved in cholesterol biosynthesis, presumably through sterol regulatory element-binding protein 2 (SREBP2).  In addition, we found that both LPC induced adhesion molecules, cytokines, and chemokines in HAECs, which are classical markers for endothelial activation.  Moreover, LPC transdifferentiated HAECs into innate immune cells including induction of potent DAMP receptors, such as CD36, T cell co-stimulation receptors and MHC-II molecules.