Soluble VEGFR-1 (sVEGFR-1) acts both as a decoy receptor for VEGFs and as an extracellular matrix protein for 51 integrin. A sVEGFR-1-derived peptide that interacts with 51 integrin promotes angiogenesis. However, canonical signal downstream integrin activation is not induced, resulting into lack of focal adhesion maturation. We performed a gene expression profile of endothelial cells adhering on sVEGFR-1 compared to that of cells adhering on fibronectin, the principal 51 integrin ligand. Three protein kinase-C substrates, adducin, MARCKS, and radixin were differently modulated. Adducin and MARCKS were less phosphorylated whereas radixin was higher phosphorylated in sVEGFR-1 adhering cells, the latter leading to prolonged small GTPase Rac1 activation and induction of a pathway involving the heterotrimeric G protein 13. Altogether, our data indicated endothelial cell acquisition of an highly motile phenotype when adherent on sVEGFR-1. Finally, we indicated radixin as accountable for the angiogenic effect of 51 integrin interaction with sVEGFR-1 that in turn depends on an active VEGF-A/VEGFR-2 signaling.
Endothelial cell adhesion to soluble vascular endothelial growth factor receptor-1 triggers a cell dynamic and angiogenic phenotype.
Specimen part
View SamplesTcl1 is known to be involved in survival, proliferation and differentiation of human lymphocytes and mouse embryonic stem cells. Loss of Tcl1 gene in the KO mouse model affects skin integrity inducing alopecia and ulcerations.
T Cell Leukemia/Lymphoma 1A is essential for mouse epidermal keratinocytes proliferation promoted by insulin-like growth factor 1.
Specimen part
View SamplesInflammatory mediators play a role in the pathogenesis/progression of chronic heart failure (CHF). The aim of the present study was to identify diagnostic/prognostic markers and gene expression profiles of CHF vs control.
Gene expression profiles in peripheral blood mononuclear cells of chronic heart failure patients.
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View SamplesEarly-passage (<10 passages) cultures of melanoma cells from metastatic lymph node lesions and normal adult melanocytes explanted in parallel from the adjacent, non-involved skin of 5 patients were compared by cDNA arrays. Differences between normal and neoplastic counterparts were then assessed upon adjustment for individual factors.
A melanoma immune response signature including Human Leukocyte Antigen-E.
Sex, Specimen part
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Identification of key regions and genes important in the pathogenesis of sezary syndrome by combining genomic and expression microarrays.
Specimen part, Disease
View SamplesThis study used tumour and paired normal samples from 28 Szary Syndrome (SS) patients to define recurrent regions of chromosomal aberrations. Our data identified recurrent losses of 17p13.2-p11.2 and 10p12.1-q26.3 occurring in 71 and 68% of cases respectively; common gains were detected for 17p11.2-q25.3 (64%) and chromosome 8/8q (50%). Moreover, we identified novel genomic lesions recurring in more than 30% of tumours: loss of 9q13-q21.33 and gain of 10p15.3-10p12.2. In the Szary Syndrome cases analysed, we could find several small and few large Uniparental Disomies involving interstitial or telomeric regions of LOH occurring mainly for chromosome 10 and to a lesser extent for chromosome 9 and 17. In the attempt to correlate Copy Number data and clinical parameters we find a relationship between complex pattern of chromosomal aberrations, involving at least three recurrent Copy Number alterations, and shorter survival. Integrating mapping and transcriptional data we were able to identify a total of 113 deregulated transcripts in aberrant chromosomal regions that included cancer related genes such as members of the NF-kB pathway (BAG4, BTRC, NKIRAS2, PSMD3, TRAF2) that might explain its constitutive activation in CTCL. Matching this list of genes with those discriminating patients with different survival times we identify several common candidates that might exert critical roles in Szary Syndrome, like BUB3 and PIP5K1B.
Identification of key regions and genes important in the pathogenesis of sezary syndrome by combining genomic and expression microarrays.
Specimen part, Disease
View SamplesTo understand which genes acts downstream AtHB1 affecting hypocotyl growth in Arabidopsis thaliana, we performed transcriptional profiles of 4-day-old seedlings grown in a short-day regime comparing wild-type with athb1-1 mutant plants. These results show that some of the AtHB1-regulated genes modulate cell elongation, particularly cell wall composition and elongation, or encode proteins that serve as a source of carbon, nitrogen, and sulfur for early seedling growth. Overall design: RNA-Seq data for 4-day-old wild-type (Col-0) and athb1-1 mutant seedlings grown under short-day conditions. Biological triplicates were performed for each genotype analyzed.
Arabidopsis thaliana HomeoBox 1 (AtHB1), a Homedomain-Leucine Zipper I (HD-Zip I) transcription factor, is regulated by PHYTOCHROME-INTERACTING FACTOR 1 to promote hypocotyl elongation.
Subject
View SamplesTo understand the fruit changes and mechanisms involved in the compatible grapevine-virus interaction, we analyzed the berry transcriptome in two stages of development (veraison and ripening) in the red wine cultivar Cabernet Sauvignon infected with Grapevine leaf-roll-associated virus-3 (GLRaV-3). Analysis of global gene expression patterns indicate incomplete berry maturation in infected berries as compared to uninfected fruit suggesting viral infection interrupts the normal berry maturation process.
Compatible GLRaV-3 viral infections affect berry ripening decreasing sugar accumulation and anthocyanin biosynthesis in Vitis vinifera.
Age, Specimen part
View SamplesBoron is an essential micronutrient for plants and is taken up in the form of boric acid (BA). Despite this, a high BA concentration is toxic for the plants, inhibiting root growth and is thus a significant problem in semi-arid areas in the world. In this work, we report the molecular basis for the inhibition of root growth caused by boron. We used microarrays to detail the global gene expression underlying boron toxicity in roots.
A molecular framework for the inhibition of Arabidopsis root growth in response to boron toxicity.
Specimen part, Treatment
View SamplesWe demonstrate that the versatile environmental bacterium Pseudomonas aeruginosa adapts a virulence phenotype after serial passage in Galleria mellonella as an invertebrate model host. The virulence phenotype was not linked to the acquisition of genetic variations and was sustained for several generations, despite cultivation of the ex vivo virulence-adapted P. aeruginosa cells under non-inducing rich medium conditions. Transcriptional reprogramming seemed to be induced by a host-specific food source as reprogramming was also observed upon cultivation of P. aeruginosa in medium supplemented with polyunsaturated long-chain fatty acids. Methods : mRNA profiles were generated for Pseudomonas aerugionsa samples derived from LB-cultures grown to an OD600 =2. The removal of ribosomal RNA was performed using the Ribo-Zero Bacteria Kit (Illumina) and cDNA libraries were generated with the ScriptSeq v2 Kit (Illumina) . The samples were sequenced in single end mode on an Illumina HiSeq 2500 device and mRNA reads were trimmed and mapped to the NC_008463.1 (PA14) reference genome from NCBI using Stampy pipeline with defaut settings. Overall design: Isolate CH2658 was subjected to in vivo and in vitro evolution experiments in this study. This isolate was obtained from the lab of G. Gastmeier, Charite Berlin, Germany. The in vivo passages (using G. mellonella) are named CH2658 I-IV corresponding to passages 1 4. The last passage CH2658 IV corresponds to the “evolved strain” and was passaged in LB (four days, two passages a day) to generate revertants which are referred to as CH2658 Rev1-4 corresponding to samples from day1-4. The last passage CH2658 Rev4 is called “revertant”. Additionally, the clinical isolate was passaged under in vitro conditions in the presence of linolenic acid (Roth) with (CH2658 Lil+P) and without paraffin (CH2658 Lil). As controls, CH2658 was passaged in LB (CH2658 LB) and in LB supplemented with paraffin (CH2658 LB+P). The in vitro passage experiment was conducted for four days and two passages a day.
Establishment of an induced memory response in Pseudomonas aeruginosa during infection of a eukaryotic host.
Subject
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