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Transcriptional profiling of a novel pro-angiogenic small molecule phthalimide neovascular factor 1 (PNF1)

ABSTRACT: We generated the transcriptional regulatory footprint of phthalimide neovascular factor 1 (PNF1)—a novel synthetic small molecule that exhibits significant in vitro endothelial potency and significant in vivo microvascular network expansion—by performing comparative microarray analysis on PNF1-stimulated (versus control) human microvascular endothelial cells (HMVEC) spanning 1-48 h post-supplementation. We subsequently applied network analysis tools (including substantial libraries of information regarding known associations among network components) to elucidate key signaling components and pathways involved in the PNF1 mechanism-of-action. We identified that PNF1 first induces function of the tumor necrosis factor-alpha (TNF-α) signaling pathway, which in turn affects transforming growth factor-beta (TGF-β) signaling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE17119 | GEO | 2009/07/17

SECONDARY ACCESSION(S): PRJNA119715

REPOSITORIES: GEO

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Transcriptional profiling of a novel pro-angiogenic small molecule phthalimide neovascular factor 1 (PNF1)

Project description:We generated the transcriptional regulatory footprint of phthalimide neovascular factor 1 (PNF1)—a novel synthetic small molecule that exhibits significant in vitro endothelial potency and significant in vivo microvascular network expansion—by performing comparative microarray analysis on PNF1-stimulated (versus control) human microvascular endothelial cells (HMVEC) spanning 1-48 h post-supplementation. We subsequently applied network analysis tools (including substantial libraries of information regarding known associations among network components) to elucidate key signaling components and pathways involved in the PNF1 mechanism-of-action. We identified that PNF1 first induces function of the tumor necrosis factor-alpha (TNF-α) signaling pathway, which in turn affects transforming growth factor-beta (TGF-β) signaling. HMVEC (Cambrex, Walkersville, MD, USA) were cultured in endothelial growth medium 2-microvascular (bulletkit, BioWhittaker, Walkersville, MD, USA) supplemented as directed with 5% fetal bovine serum. The cells (passage 9) were plated at 2.5 x 104 cells/cm2 at 37 degrees Celsius in a humidified chamber with 5% carbon dioxide. They were grown to confluence. After confluence, medium was refreshed, and 30 µM PNF1 or 0.6% dimethyl sulfoxide (DMSO) vehicle control was added to the sample. Total RNA from the PNF1 (n=1 at each timepoint) and control (n=1 at each timepoint) samples was isolated 1, 2, 4, 8, 16, 24 and 48 h post-supplementation using an RNeasy kit (Qiagen, Inc., Valencia, CA, USA) according to the manufacturer's protocol.

2009-07-17 | E-GEOD-17119 | biostudies-arrayexpress

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Transcription profiling of human HMVEC cells treated with vascular endothelial growth factor, anthrax edema toxin, and an Epac activator

Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT); Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment. Experiment Overall Design: Gene expression was measured 4 hours after treatment with VEGF, VEGF + 8CPT, VEGF + ET or mock treatment. Each sample contained one replicate.

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Project description:Endothelial cells (EC) were obtained from commercial source (Lonza), expanded and culture until passage 3. HMVEC-LBI correspond to lung microvascular endothelial cells, HPAEC to lung macrovascular endothelial cells, HAEC to cardiac macrovascular endothelial cells and HMVEC-C to cardia microvascular endothelial cells. These cells presented different capacity to generate endothelial microvesicles. The objective of the study was to identify differentially genes between these cells to understand this difference. Total RNA was extracted using the mirVana miRNA Isolation Kit (Ambion), according to the manufacturer’s recommendations. Cy3-CTP labeled RNA was prepared according to standard Agilent protocol from 400ng total RNA. The hybridization was performed for 17 hrs at 65°C. cRNA labeling and hybridization performance were performed and all parameters checked were found within the manufacturers specifications. Arrays were scanned as described in the manufacturers’ protocol. Signal intensities on 20 bit tiff images were calculated by Feature Extraction software (FE, Version 8.5; Agilent Technologies). Data analyses were conducted with GeneSpring GX software (Vers.12.6; Agilent Technologies)

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Project description:To identify endothelial cell (EC)-enriched long noncoding RNAs (lncRNAs), gene expression analysis was conducted on two EC cell types and 4 non-EC cell types. Specifically, the EC cell types were human umbilical vein endothelial cells (HUVEC) and human dermal microvascular endothelial cells (HMVEC). The 4 non-EC cell types were human aortic smooth muscle cells (HASMC), Fibroblasts, Hepatocytes, and keratinocytes. Of the 23 155 putative lncRNAs represented in the custom lncRNA microarrays, 18 524 lncRNAs were found to be expressed above the 20% percentile in at least one cell type. Importantly, 28 EC-enriched lncRNAs were identified in common between HUVEC and HMVEC with 28 and 59 enriched uniquely in either HUVEC or HMVEC, respectively. Of interest, STEEL, an EC-enriched lncRNA was identified and its role in EC biology was further characterized.

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Project description:This study employed Affymetrix GeneChips to profile transcriptome of human pulmonary microvascular endothelial cells (HMVEC-L) treated with PBEFsiRNA to gain insight into transcriptional regulations of PBEF on the endothelial function. We isolated and labeled mRNAs from PBEF siRNA transfected HMVEC-L and hybridized them to Affymetrix GeneChip HG-U133 plus 2. Differentially expressed genes and canonical pathways were analyzed. Expressions of selected genes were validated by RT-PCR or western blotting. Several important themes are emerged from this study. First, PBEF induces the upregulation and downregulation of multiple genes in the endothelium. Expression of 373 genes were increased and 64 genes decreased by at least 1.3 fold in the PBEFsiRNA treated group compared to the control group of PBEFscRNA treated HMVEC-L. Second, the microarray results confirmed some previous reports of PBEF mediated gene expressions in some pathways but provided a more complete repertoire of molecules in those pathways. Third, most of affected canonical pathways or differentially expressed genes in PBEF siRNA treated HMVEC-L over their controls have not previously been reported to be PBEF-responsive. Our first transcriptome analysis of human pulmonary microvascular endothelial cells treated with PBEFsiRNA has provided important insights into the transcriptional regulation of gene expression in HMVEC-L cells by PBEF. Further in-depth follow-up analysis of the transcriptional regulation reported in this study may shed light on molecular mechanisms underlying PBEF mediated endothelial functions and dysfunctions in the physiology and the pathogenesis of inflammatory conditions, cancer, diabetes, coronary heart disease and provide new leads of therapeutic targets to those diseases.

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