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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNAi profiling of human lymphatic endothelial cells after knockdown of Prox1 and/or NR2F2

ABSTRACT: Gene expression profiles of primary lymphatic endothelial cells (LECs) isolated from human foreskin were analyzed after siRNA-mediated knockdown of control (firefly luciferase), Prox1, NR2F2 or Prox1/NR2F2 for 48 hours. Experiment Overall Design: Passage five human lymphatic endothelial cells (LECs) were cultured on fibronectin (10 Î¼g/ml)-coated plates in a complete media (EBM, 20% FBS supplemented with 10 Î¼g/ml hydrocortisone acetate, 25 ug/ml cAMP and antibiotics). LECs were harvested and electorporated with siRNA duplexes for 48 hours with siRNA duplexes against either firefly luciferase(control), Prox1, NR2F2 or Prox1/NR2F2. Total RNA was purified using Tri-reagent and was subjected to microarray analysis. Experiment Overall Design:

ORGANISM(S): Homo sapiens

SUBMITTER: Young-Kwon Hong

PROVIDER: E-GEOD-12846 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiles of lymphatic endothelial cells after knockdown of Prox1 and/or NR2F2

Project description:Gene expression profiles of primary lymphatic endothelial cells (LECs) isolated from human foreskin were analyzed after siRNA-mediated knockdown of control (firefly luciferase), Prox1, NR2F2 or Prox1/NR2F2 for 48 hours.

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ROLE OF FATTY ACID ß-OXIDATION IN LYMPHANGIOGENESIS

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Atlas of lymphangiogenesis [scATAC-Seq]

Project description:During development, lymphatic vasculature forms as a second and distinct network that derives from embryonic blood vessels. Transdifferentiation of venous endothelial cells into specified lymphatic endothelial cells (LECs) is the first step in this process. Transdifferentiation and specification of LEC fate requires Prox1, but how Prox1 regulates transdifferentiation and differentiation is not fully understood. We present a single cell transcriptomic atlas of lymphangiogenesis spanning four key developmental stages that reveals new markers and functional regulators of lymphatic development. We extend this to comprehensively profile single cell transcriptomic and chromatin changes controlled by Prox1 using zygotic prox1a mutants, which form lymphatics that then dedifferentiate. Combining this with single cell analysis of Prox1-null, double prox1a/prox1b maternal zygotic mutants, we reveal in depth the role of Prox1 in control of LEC fate specification and differentiation. This resource reveals dual and progressive functions for Prox1, blocking blood vascular and hematopoietic fate while simultaneously up-regulating a small number of early acting genes that include tspan18a/b and lgals3a/b which are essential for lymphangiogenesis. This embryonic developmental resource will serve as a baseline to better understand both developmental and pathological lymphangiogenesis in the future. [Citations in sample metadata correspond to reference numbers in the associated publication.]

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Project description:Panc1 (human pancreatic adenocarcinoma cells) cells were transfected with control siRNA (targeting firefly luciferase, siLuc) or siRNA targeting GLI1 (siGLI1, Pool of four siRNAs). 72h following transfection, RNA was prepared for array analysis.

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Lymphatic endothelial cell identity is controlled by a GATA2 bound enhancer [RNA-seq]

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Project description:Human Notch1 intracellular domain (NICD) was overexpressed in human primary lymphatic endothelial cells (LECs) for 10 and 24 hours by adenovirus. A GFP-control adenovirus-infected cells (24hours) and uninfected cells were also analysed as controls. Total RNAs were harvested and subjected to Affymetrix U133A microarray. Human primary lymphatic endothelial cells (LECs) were isolated from human foreskin and cultured and expanded to population passages 5~6. Healthy subconfluent primary LECs were infected with adenovirus expressing human Notch1 intracellular domain (NICD) for 10 or 24 hours. In parallel, LECs were also infected with a GFP-expressing control adenovirus for 24 hours. Uninfected LECs were also used as a negative control in the same experiments

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