Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic characterization of media conditioned by embryonic sympathetic ganglia and dorsal root ganglia

ABSTRACT: Embryonic malignant transformation is concomitant to organogenesis, often affecting multipotent and migratory progenitors. Neuroblastoma (NB) is an emblematic example, arising from neural crest progenitors and characterized by a high heterogeneity and a widely disseminated clinical presentation. Metastatic triggers from the embryonic environment are suspected but yet unknown due to limited investigation access in patients and current models. Using combinations of ex vivo and in vivo models mimicking the embryonic context coupled to proteomic and transcriptomic analyses, we identify Olfactomedin1 (OLFM1) released by sympathetic derivatives at the core of a gene program promoting NB cells decohesion, primary tumor escape and dissemination.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Gallus Gallus (chicken) Mus Musculus (mouse)

TISSUE(S): Embryo

SUBMITTER: Yohann Couté

LAB HEAD: Yohann Couté

PROVIDER: PXD027499 | Pride | 2022-05-04

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Similar Datasets

The role of miRNAs in neuroblastoma tumor development

Project description:Neuroblastoma (NB) is an embryonic tumor arising from immature sympathetic nervous system progenitor cells. MYCN and ALK are driver oncogenes both of which are specifically expressed during early neurogenesis. This is in line with the assumption that NB arises through disruption of normal developmental processes. MYCN has a broad impact on the tumor phenotype; however, the details of the MYCN driven oncogenic program are far from clear. In recent studies we demonstrated that MYCN drives the expression of a defined set of miRNAs that tightly control the expression of several key MYCN target genes, including several components of the TGFÎ² signaling pathway. In order to gain further insight into the role of miRNAs in NB initiation and progression, we evaluated miRNA profiles of hyperplastic ganglia and tumors isolated from MYCN transgenic mice.

2014-10-01 | E-MTAB-2618 | biostudies-arrayexpress

Transcription profiling of trigeminal ganglia of Brn3a knockout and wild type mice to determine the regulatory targets of transcription factor Brn3a.

Project description:Mice lacking the POU-domain transcription factor Brn3a exhibit marked defects in sensory axon growth and abnormal sensory apoptosis. We have determined the regulatory targets of Brn3a in the developing trigeminal ganglion using microarray analysis of Brn3a mutant mice. These results show that Brn3 mediates the coordinated expression of neurotransmitter systems, ion channels, structural components of axons and inter- and intracellular signaling systems. Loss of Brn3a also results in the ectopic expression of transcription factors normally detected in earlier developmental stages and in other areas of the nervous system. Target gene expression is normal in heterozygous mice, consistent with prior work showing that autoregulation by Brn3a results in gene dosage compensation. Detailed examination of the expression of several of these downstream genes reveals that the regulatory role of Brn3a in the trigeminal ganglion appears to be conserved in more posterior sensory ganglia but not in the CNS neurons that express this factor. Experiment Overall Design: Microarrays used to compare the patterns of gene expression in the trigeminal ganglia of Brn3a knockout and wild-type mice. Embryonic day 13.5 (E13.5) was chosen because at this point in development mutant mice exhibit major defects in sensory axon growth, but have yet to undergo the period of extensive sensory neuron death associated with later stages.

2007-11-01 | E-GEOD-3895 | biostudies-arrayexpress

Embryonic neural crest cell derivatives release pro-metastatic cues driving neuroblastoma dissemination in an avian disease model

Project description:Embryonic malignant transformation is concomitant to organogenesis, often affecting multipotent and migratory progenitors. Neuroblastoma (NB) is an emblematic example, arising from neural crest progenitors and characterized by a high heterogeneity and a widely disseminated clinical presentation. Metastatic triggers from the embryonic environment are suspected but yet unknown due to limited investigation access in patients and current models. Using combinations of ex vivo and in vivo models mimicking the embryonic context coupled to proteomic and transcriptomic analyses, we identify Olfactomedin1 (OLFM1) released by sympathetic derivatives at the core of a gene program promoting NB cells decohesion, primary tumor escape and dissemination. This OLFM signature discriminates metastatic from localized stages in NB patient cohorts. Finally, we report an extended tumor cell escape gene signature of disseminated forms specifically shared by cancers with neural-crest origin, revealing a sustained embryonic imprint of the lineage of origin, manifested in the metastatic properties of malignant cells.

2022-03-09 | GSE169280 | GEO

Aplysia Pleural Ganglia 24 Hours After Long-Term Habituation Training

Project description:We used a custom-designed microarray and qPCR to characterize the persistent transcriptional response to long-term habituation training in the marine mollusk Aplysia californica. Aplysia were exposed to either 3 days of spaced long-term habituation training (10 rounds of stimulation/day; each round = 15 min brushing at a 10s ISI; 15 min rest between rounds); a matched set of controls was not exposed to any brushing (n = 8/group). While reflex responsiveness remained stable in controls, trained animals exhibited a large reduction in siphon-withdrawal duration that was evident at stimulation sites across the entire dorsal surface of the body (head, tail, and siphon). This habituation was retained for at least 24 hours after the end of training. Immediately after 24 hour retention tests, pleural ganglia were harvested from each trained animal and its matched control. The pleural ganglia contain the VC nociceptors, which we confirmed are activated by the brush stimulus used to produce habituation. Microarray analysis from 8 biological replicates suggests that long-term habituation training persistently regulates 21 transcripts. We used qPCR to test a subset of these transcripts and found persistent regulation of an putative Aplysia cornichon homolog. Between-subjects comparison of a trained animal to a matched control (matching based on duration of pre-test responsiveness). Conducted with 8 biological replicates, meaning 8 arrays, each comparing 1 trained and 1 matched control.

2014-07-16 | E-GEOD-59448 | biostudies-arrayexpress

Increased Hemodynamic Load in Early Embryonic Stages Alters Endocardial to Mesenchymal Transition

Project description:Normal blood flow is essential for proper heart formation during embryonic development, as abnormal hemodynamic load (blood pressure and shear stress) results in cardiac defects seen in congenital heart disease. However, the progressive detrimental remodeling processes that relate altered blood flow to cardiac defects remain unclear. Outflow tract banding was used to increase hemodynamic load in the chicken embryo heart between Hamburger and Hamilton stages 18 and 24. Increased hemodynamic load induced increased cell density in outflow tract cushions, fewer cells along the endocardial lining, endocardium junction disruption, and altered periostin expression as measured by confocal microscopy analysis. Proteomic mass-spectrometry analysis quantified altered protein composition after banding.

2018-10-26 | PXD005362 | Pride

11q deletion or ALK activity curbs DLG2 expression to maintain an undifferentiated state in neuroblastoma.

Project description:High-risk 11q deleted neuroblastomas (NBs) typically display an undifferentiated/poorly differentiated morphology. NB is thought to develop from Schwann cell precursors (SCPs) and un-differentiated neural crest derived cells (NCC). It is therefore vital to understand the mechanisms involved in the block of differentiation. We showed that an important and novel role for oncogenic ALK-ERK1/2-SP1 signaling may be the maintenance of an undifferentiated state of transformed NC-derived progenitors that is achieved by repression of DLG2, a tumor suppressor in NB. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors (SCP) become chromaffin cells of the adrenal gland. The importance of SP1 and DLG2 in this process is highlighted by our findings that restoring DLG2 expression spontaneously drives NB differentiation. Further, genetic analysis of high-risk 11q deletion NB patient identified genetic lesions in the DLG2 gene, Our data also suggest that further exploration of other ‘bridge genes’ may help to better understand the mechanisms underlying the differentiation of NC-derived progenitors and their contribution to NB.

2020-11-25 | PXD017946 | Pride

mRNA-seq data of embryonic chicken digits

Project description:Morphological characters are the result of developmental gene expression. Hence the identity of a character is ultimately grounded in the gene regulatory network directing development and thus whole genome gene expression data can provide evidence about character identity. Here we use transcriptomic data to address one of the most enduring paradoxes in evolutionary biology, the identity of the avian wing digits. Deep Sequencing of mRNA from embryonic chicken digits is performed and the gene expression profiles are analyzed. Analysis of mRNA-seq data from 16 samples of chicken digits covering two embryonic stages.

2011-09-07 | E-GEOD-28156 | biostudies-arrayexpress

Transcription profiling of Xenopus dorsal root ganglia conditioned in vitro vs freshly dissected control

Project description:Axonal regeneration is enhanced by prior conditioning peripheral nerve lesions. Here we show that Xenopus dorsal root ganglia (DRGs) with attached peripheral nerves (PN-DRGs) can be conditioned in vitro, thereafter showing enhanced axonal growth in response to neurotrophins, similar to preparations conditioned by axotomy in vivo. In contrast to freshly dissected preparations, conditioned PN-DRGs show abundant neurotrophin-induced axonal growth in the presence of actinomycin D, suggesting synthesis of mRNA encoding proteins necessary for axonal elongation occurs during the conditioning period, and this was confirmed by oligonucleotide micro-array analysis.

2008-04-16 | E-MEXP-1297 | biostudies-arrayexpress

BRG1/SMARCA4 is essential for neuroblastoma cell viability through modulation of cell death and survival pathways

Project description:Neuroblastoma (NB) is a neoplasm of the sympathetic nervous system, and is the most common solid tumor of infancy. NBs are very heterogeneous, with a clinical course ranging from spontaneous regression to resistance to all current forms of treatment. High-risk patients need intense chemotherapy, and only 30-40% will be cured. Relapsed or metastatic tumors acquire multi-drug resistance, raising the need for alternative treatments. Owing to the diverse mechanisms that are responsible of NB chemoresistance, we aimed to target epigenetic factors that control multiple pathways to bypass therapy resistance. We found that the SWI/SNF-related, matrix-associated, actin- dependent regulator of chromatin, subfamily a, member 4 (SMARCA4/BRG1) was consistently upregulated in advanced stages of NB, with high BRG1 levels being indicative of poor outcome. Loss-of-function experiments in vitro and in vivo showed that BRG1 is essential for the proliferation of NB cells. Furthermore, whole genome transcriptome analysis revealed that BRG1 controls the expression of key elements of oncogenic pathways such as PI3K/AKT and BCL2, which offers a promising new combination therapy for high-risk NB Non-silencing control (NSC) or shBRG1 lentiviral vectors were transduced in the Neuroblastoma cell lines SK-N-BE(2) by triplicate. 48h post-infection, total RNA was extracted

2016-03-01 | E-GEOD-74622 | biostudies-arrayexpress

Ascl1, Nurr1 and Lmx1 convert mouse and human fibroblasts into functional dopaminergic neurons without passing through an intermediate precursor state

Project description:Lineage-specific transcription factors, which drive cellular identity during embryogenesis, have been shown to convert cell fate when express ectopically in heterologous cells. Herein, we screened the key molecular factors governing the dopaminergic neuronal specification during brain development for their ability to generate similar neurons directly from mouse and human fibroblasts. Remarkably, we found a minimal set of three factors Mash1, Nurr1 and Lmx1a/b able to elicit such cellular reprogramming. Molecular and transcriptome studies showed reprogrammed DA neurons to faithfully recapitulate gene expression of their brain homolog cells while lacking expression of other catecholaminergic neuronal types. Induced neurons showed spontaneous electrical activity organized in regular spikes consistent with the pacemaker activity featured by brain DA neurons. The three factors were able to elicit DA neuronal conversion in human fibroblasts from prenatal or adult fibroblasts of healthy donors and a Parkinson’s disease patient. Generation of DA induced neurons from somatic cells might have significant implications in studies of neural development, disease in vitro modeling and cell replacement therapies. We infected mouse embryonic fibroblasts (MEFs) isolated from TH-GFP knock-in mice embryos at E14.5, with lentiviruses expressing the three dopaminergic transcription factors Ascl1, Lmx1a and Nurr1. TH-GFP MEFs infected (Ind) by a pool of the three previously mentioned dopaminergic lentiviruses were shifted in a neuronal medium for 12 days and sorted for GFP-positive cells. Thus we extracted mRNA from Ind-GFP-positive cells and compared them to not infetced (NI) cells by means of RNA-microarray analysis.

2011-07-04 | E-GEOD-27174 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data