Project description:Transcriptional profiling of human umbilical vein endothelial cells following stimulation with tumour necrosis factor alpha and transforming growth factor beta singly or combined for 8 hr All stimulations were for 8 hr - TNF-α vs no cytokine; TGF-β1 vs no cytokine; TNF-α & TGF-β1 vs TNF-α alone; TNF-α & TGF-β1 vs TGF-β1 alone
Project description: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.
Project description:Endothelial inflammation is a critical contributor to atherosclerosis and is tightly regulated by mechanical and inflammatory cues. Here, we identify SWAP70 as a key mechanosensitive adaptor protein involved in endothelial inflammatory responses. Using RNA-seq analysis of human umbilical vein endothelial cells (HUVECs) under three conditions—control (KOC), TNF-α stimulation (TKOC), and TNF-α stimulation with SWAP70 knockdown (TKO)—we demonstrate that SWAP70 deficiency profoundly alters the transcriptional landscape induced by TNF-α. SWAP70 knockdown suppresses the expression of key pro-inflammatory mediators such as VCAM1, MCP1, and CXCL8. Functional enrichment analysis reveals that SWAP70 regulates inflammation-related pathways including TNF, NF-κB, and MAPK signaling. These findings suggest that SWAP70 facilitates endothelial inflammation by promoting transcriptional responses to pro-inflammatory stimuli and may serve as a regulatory hub linking disturbed flow and cytokine signaling in atherosclerosis.
Project description:Human Umbilical Vein Endothelial Cells (HUVECs) were isolated from umbilical chords by collagenase digestion and cultured to passage 3. HUVECs were pre-activated for 4 hours with TNF-alpha (10ng/ml), followed by rHDL (0.1 and 1mg/ml) treatment for a further 8 hours. RNA isolated and labeled using the Illumina total prep RNA amplification kit and analysed using the Illumina sentrix beadchip microarray HT-12 (n=3 per treatment)
Project description:Transcriptional profiling of human umbilical vein endothelial cells following stimulation with tumour necrosis factor alpha and transforming growth factor beta singly or combined for 8 hr
Project description:Intra- and extracellular metabolomics dataset of human dermal blood endothelial cells (HDBECs), human umbilical vein endothelial cells (HUVECs), human dermal lymphatic endothelial cells (HDLECs) and intestinal lymphatic endothelial cells (iLECs) in proliferation and quiescence.
Project description:We demonstrated that an abundant Collagen type I alpha 1-derived peptide inhibited collagen type I-induced endothelial cell migration in Human Umbilical Vein Endothelial Cells. We then applied mass spectrometry based proteomics to investigate the potential signalling pathways induced by collagen type I (full length), and were inhibited by the Collagen type I alpha 1-derived peptide.
Project description:Endothelial cells play many important role during development and development of diseases. Endothelial dysfunction which is commonly seen in diabetes patients is thought to be one of the first step that leads to adverse events such as retinopathy, nephropathy, and atherosclerosis. To examine to which extent TGF-beta signaling contributes to insulin-induced transcriptional responses we performed this RNAseq on Human umbilical vein endothelial cells.
