Project description:To investigate the mechanism of histamine H1 receptor (H1R)- mediated proliferation and angiogenesis of endothelial cells, mRNA profiles of HUVEC cells transduced with shNT or shH1R under histamine treatment for 9 hrs were generated by deep sequencing, in replicate, using Illumina GAIIx. We identified the upregulation of genes in several pathways including angiogenesis, proliferation and migration that could be responsible for the increased tube formation in histamine treated shNT expressing HUVEC cells
Project description:Purpose: The goal of this study is to investigate the responses of HUVECs after the stimulation of conidia of A. fumigatus Methods: HUVECs were stimulated with conidia of Aspergillus fumigatus for 2 and 6 hours. Three biological repeats of stimulated cells or un-stimulated controls were send for RNA sequencing. Results: Using an optimized data analysis workflow, we mapped about 40 million sequence reads per sample to the human genome (build hg38) and identified round 80,000 transcripts in the HUVECs upon stimulation. Conclusions: Our resutls showed the detailed analysis of HUVECs transcriptomes upton conidia of Aspergillus fumigatus stimulation.
Project description:HUVECs were stimulated and samples were prepared after 0 and 30 min. Chromatin interaction mediated by active RNA polymerase II was detected by ChIA-PET.
Project description:HUVECs were stimulated and samples were prepared after 0 and 30 min. Chromatin interaction mediated by active RNA polymerase II was detected by ChIA-PET. Samples were made afrer 0 and 30 min after TNF alpha stimulation.
Project description:IL-6 family cytokines as OSM and CNTF modify angiogenesis to different degree. This study investigates to which extend treatment of endothelial cells with those cytokines can modify VEGF induced angiogenic reactions. Human umbilical vein endothelial cells (HUVECs) were stimulated for 24h by cytokines followed by RNA harvesting and processed for RNA sequencing.
Project description:Purpose: In recent years, research has revealed the role of microRNAs (miRs) as important regulators of endothelial function. Notably, miR-125a is upregulated in the blood of patients with acute vascular diseases. Since miRNAs act out their function in networks, we aimed at investigating the presence of a miR-125a-related network regulating the endothelial barrier. Method: We investigated transcriptional changes of human umbilical cord endothelial cells (HUVEC) after miR-125a overexpression in an acute inflammatory in-vitro setting using Next Generation Sequencing. Briefly, primary HUVECs from five different donors were transfected either with hsa-miR-125a-5p or negative control (NC). After transfection HUVECs were cultivated for 18 hours and stimulated with TNF (25 ng/ml) for additional 6 hours. We compared the following groups: NC (18047-0001, 18047-0002, 18047-0003, 18047-0004, 18047-0005) versus miR125a: (18047-0006, 18047-0007, 18047-0008, 18047-0009, 18047-0010) Results: MiR-125a overexpression in inflammatory activated HUVECs significantly altered gene expression of 468 genes (FC: +1.25 to -1.25 p<0.01). We found eight potential miR-125a direct target genes involved in endothelial barrier function.
Project description:Hantaan virus (HTNV) causes hemorrhagic fever with renal syndrome (HFRS). Previous studies have identified interferon stimulate genes (ISGs) play important roles in viral infection. However, the role of ISGs in HTNV infection is unclear. In this study, we observed the alteration of gene expression in HUVECs infected with HTNV compared with mock infected control and found considerable changes in mRNA and lncRNA profiles.
Project description:Using human umbilical vein endothelial cells (HUVECs) as cell models, the present study aims to explore the differential miRNAs in influenza virus-infected ECs and analyze their target genes involved in EC permeability regulation. As the results showed, permeability increased and F-actin cytoskeleton reorganized after HUVECs infected with influenza A virus (CA07 or PR8) at 30 MOI. most of these miRNAs were down-regulated after flu infection. It has been reported that PKC, Rho/ROCK, HRas/Raf/MEK/ERK, and Ca2+/CaM pathways are activated by flu infection and play important roles in permeability regulation.