Time 24 hr to 0 hr
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE778 | GEO | 2003/11/25
SECONDARY ACCESSION(S): PRJNA89813
REPOSITORIES: GEO
Similar Datasets
Project description:Four dye swap replicates were performed with material derived 6 hours after stimulation of HUVECs with PMA and RMAC11 hybridised to material obtained at time 0 hours. Keywords = angiogenesis Keywords = HUVEC Keywords = in vitro Keywords = capillary tube Keywords: repeat sample
2003-11-25 | GSE777 | GEO
Project description:This is a time course experiment with 4 - 6 slides per time point where all samples were hybridised to time zero. The microarray slides were scanned using a GenePix 4000B Scanner (Axon Instruments, Foster City, CA, USA). The “SPOT” software package (CSIRO) was used to identify spots and subtract backgrounds. The extracted information was normalised using the “Statistics in Microarray Analysis" (SMA) open source R package. Scaled print tip group lowes normalisation was performed for each slide and replicate slides were scaled to each other. The cDNAs used in this microarray were identified as part of collaborative project between the IMVS and Bionomics Limited. The project aims were to identify genes up-regulated during in vitro capillary tube formation as targets for angiogenesis-based therapeutics. Any requests for further information regarding the data generated from this collaboration should be directed to Bionomics Limited (www.bionomics.com.au) at the following address: Bionomics Limited 31 Dalgleish Street Thebarton, South Australia Australia, 5031 Phone: 618 8354 6104 Fax: 618 8354 6199 Email: busdev@bionomics.com.au This SuperSeries is composed of the SubSeries listed below.
2003-11-25 | GSE779 | GEO
Project description:This is a time course experiment with 4 - 6 slides per time point where all samples were hybridised to time zero. The microarray slides were scanned using a GenePix 4000B Scanner (Axon Instruments, Foster City, CA, USA). The â??SPOTâ?? software package (CSIRO) was used to identify spots and subtract backgrounds. The extracted information was normalised using the â??Statistics in Microarray Analysis" (SMA) open source R package. Scaled print tip group lowes normalisation was performed for each slide and replicate slides were scaled to each other. The cDNAs used in this microarray were identified as part of collaborative project between the IMVS and Bionomics Limited. The project aims were to identify genes up-regulated during in vitro capillary tube formation as targets for angiogenesis-based therapeutics. This SuperSeries is composed of the following subset Series: GSE767: time 0.5 hr to 0 hr GSE771: time 3 hr to 0 hr GSE777: time 6 hr to 0 hr GSE778: time 24 hr to 0 hr Any requests for further information regarding the data generated from this collaboration should be directed to Bionomics Limited (www.bionomics.com.au) at the following address: Bionomics Limited 31 Dalgleish Street Thebarton, South Australia Australia, 5031 Phone: 618 8354 6104 Fax: 618 8354 6199 Email: busdev@bionomics.com.au Refer to individual Series
2010-06-05 | E-GEOD-779 | biostudies-arrayexpress
Project description:Six dye swap replicates were performed with material derived 0.5 hour after stimulation of HUVECs with PMA and RMAC11 hybridised to material obtained at time 0 hours. Keywords: repeat sample
2003-11-26 | GSE767 | GEO
Project description:Four dye swap replicates were performed with material derived 3 hour after stimulation of HUVECs with PMA and RMAC11, hybridised to material obtained at time 0 hours. Keywords: repeat sample
2003-11-25 | GSE771 | GEO
Project description:Angiogenesis is a complex multicellular process requiring the orchestration of many events including migration, alignment, proliferation, lumen formation, remodeling, and maturation. Such complexity indicates that not only individual genes but also entire signaling pathways will be crucial in angiogenesis. To define an angiogenic blueprint of regulated genes, we utilized our well-characterized three-dimensional collagen gel model of in vitro angiogenesis, in which the majority of cells synchronously progress through defined morphological stages culminating in the formation of capillary tubes. We developed a comprehensive three-tiered approach using microarray analysis, which allowed us to identify genes known to be involved in angiogenesis and genes hitherto unlinked to angiogenesis as well as novel genes and has proven especially useful for genes where the magnitude of change is small. From a screen of miRNAs altered in in vitro angiogenesis we selected a subset that are predicted to target junctional molecules. MiR-27a, was rapidly downregulated upon stimulation of in vitro angiogenesis and its level of expression is reduced in neo-vessels in vivo. The downregulation of miR-27a was essential for angiogenesis since ectopic expression of miR-27a blocked capillary tube formation and angiogenesis. MiR-27a targets the junctional, endothelial specific cadherin, VE-cadherin. Consistent with this, vascular permeability to VEGF in mice is reduced by administration of a general miR-27 inhibitor. To determine that VE-cadherin was the dominant target of miR-27a function we used a novel technology with M-bM-^@M-^\BlockmirsM-bM-^@M-^], inhibitors that bind to the miR-27 binding site in VE-cadherin. The Blockmir CD5-2 demonstrated specificity for VE-cadherin and inhibited vascular leak in vitro and in vivo. Furthermore CD5-2 reduced oedema, increased capillary density and potently enhanced recovery form ischemic limb injury in mice. The Blockmir technology offers a refinement in the use of miRNAs especially for therapy. Further, targeting of endothelial junctional molecules by miRNAs has clinical potential especially in diseases associated with vascular leak. A microRNA microarray was performed to investigate miRNAs that were regulated during capillary tube formation and which could potentially be used as an M-bM-^@M-^XangiogenicM-bM-^@M-^Y miRNA profile. RNA was isolated from cells harvested at specific time points, previously identified as stages where major morphological changes are taking place18. These include 0.5 hour (invasion), 3 hours (migration), 6 hours (vacuole coalescence and lumen formation), 12 hours (lumen formation) and 24 hours (tube maturation).
2013-09-30 | E-GEOD-50437 | biostudies-arrayexpress
Project description:Angiogenesis is a complex multicellular process requiring the orchestration of many events including migration, alignment, proliferation, lumen formation, remodeling, and maturation. Such complexity indicates that not only individual genes but also entire signaling pathways will be crucial in angiogenesis. To define an angiogenic blueprint of regulated genes, we utilized our well-characterized three-dimensional collagen gel model of in vitro angiogenesis, in which the majority of cells synchronously progress through defined morphological stages culminating in the formation of capillary tubes. We developed a comprehensive three-tiered approach using microarray analysis, which allowed us to identify genes known to be involved in angiogenesis and genes hitherto unlinked to angiogenesis as well as novel genes and has proven especially useful for genes where the magnitude of change is small. From a screen of miRNAs altered in in vitro angiogenesis we selected a subset that are predicted to target junctional molecules. MiR-27a, was rapidly downregulated upon stimulation of in vitro angiogenesis and its level of expression is reduced in neo-vessels in vivo. The downregulation of miR-27a was essential for angiogenesis since ectopic expression of miR-27a blocked capillary tube formation and angiogenesis. MiR-27a targets the junctional, endothelial specific cadherin, VE-cadherin. Consistent with this, vascular permeability to VEGF in mice is reduced by administration of a general miR-27 inhibitor. To determine that VE-cadherin was the dominant target of miR-27a function we used a novel technology with “Blockmirs”, inhibitors that bind to the miR-27 binding site in VE-cadherin. The Blockmir CD5-2 demonstrated specificity for VE-cadherin and inhibited vascular leak in vitro and in vivo. Furthermore CD5-2 reduced oedema, increased capillary density and potently enhanced recovery form ischemic limb injury in mice. The Blockmir technology offers a refinement in the use of miRNAs especially for therapy. Further, targeting of endothelial junctional molecules by miRNAs has clinical potential especially in diseases associated with vascular leak.
2013-09-30 | GSE50437 | GEO
Project description:Human umbilical vein endothelial cells (HUVECs) formed capillary structures when co-cultured with normal human dermal fibroblasts (NHDFs). HUVEC competence and NHDF supportiveness of cord formation were found to be highly cell-passage dependent with the early passage cells forming more angiogenic cord structures. We thus profiled gene expression in NHDFs with different passages to understand the molecular mechanisms underlying the in vitro angiogenesis control. Keywords: Time course
2008-05-13 | GSE11418 | GEO
Project description:Class IIa histone deacetylases (HDACs) are signal-responsive regulators of gene expression involved in vascular homeostasis. To investigate the differential role of class IIa HDACs for the regulation of angiogenesis, we used siRNA to specifically suppress the individual HDAC isoenzymes. Among the HDAC isoforms tested, silencing of HDAC5 exhibited a unique pro-angiogenic effect evidenced by increased endothelial cell migration, sprouting and tube formation. Consistently, overexpression of HDAC5 decreased sprout formation, indicating that HDAC5 is a negative regulator of angiogenesis. The anti-angiogenic activity of HDAC5 was independent of MEF2 binding and its deacetylase activity, but required a nuclear localization indicating that HDAC5 might affect the transcriptional regulation of gene expression. To identify putative HDAC5 targets, we performed microarray expression analysis. Silencing of HDAC5 increased the expression of fibroblast growth factor 2 (FGF2) and angiogenic guidance factors including Slit2. Antagonization of FGF2 or Slit2 reduced sprout induction in response to HDAC5 siRNA. ChIP assays demonstrate that HDAC5 binds to the promoter of FGF2 and Slit2. In summary, HDAC5 represses angiogenic genes, like FGF2 and Slit2, which causally contribute to capillary-like sprouting of endothelial cells. The de-repression of angiogenic genes by HDAC5 inactivation may provide a useful therapeutic target for induction of angiogenesis. Experiment Overall Design: 6 samples: 3x siSCRAMBLED transfected HUVEC (control) + 3x siHDAC5 transfected HUVEC 24h after transfection
2009-04-11 | E-GEOD-15499 | biostudies-arrayexpress
Project description:Obesity is a leading risk factor for type-2 diabetes. Diabetes often leads to the dysregulation of angiogenesis, although, the mechanism is not fully understood. Previously, long noncoding RNAs (lncRNAs) have been found to modulate angiogenesis. In this study, we asked how the expression levels of lncRNAs change in endothelial cells in response to excessive palmitic acid treatment, an obesity-like condition. Bioinformatics analysis revealed that 305 protein-coding transcripts were upregulated and 70 were downregulated, while 64 lncRNAs were upregulated and 46 were downregulated. Gene ontology and pathway analysis identified endoplasmic reticulum stress, HIF-1 signaling, and Toll-like receptor signaling as enriched after palmitic acid treatment. In addition, we newly report enrichment of AGE-RAGE signaling pathway in diabetic complications, IL-17 signaling, and cysteine and methionine metabolism by palmitic acid. One lncRNA, Colorectal Neoplasia Differentially Expressed (CRNDE), was selected for further investigation. Palmitic acid induces CRNDE expression by 1.9-fold. We observed that CRNDE knockdown decreases endothelial cell proliferation, migration, and capillary tube formation. These decreases are synergistic under palmitic acid stress. These data demonstrated that CRNDE is a regulator of endothelial cell proliferation, migration, and tube formation in response to palmitic acid, and a potential target for therapies treating the complications of obesity-induced diabetes.
2019-12-20 | GSE141126 | GEO