Gene expression data of human mesenchymal stromal cells, fibroblasts and hematopoietic progenitors
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Beatriz Burgo
PROVIDER: E-GEOD-72332 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Mesenchymal stromal cells (MSCs) derived from the BM of healthy donors (dMSCs) and myeloma patients (pMSCs) were co-cultured with the model myeloma cell line - MM.1S -, and the gene expression profile of MSCs induced by this interaction was analyzed using high density oligonucleotide microarrays. Deregulated genes in co-culture common to both d/pMSCs revealed functional involvement in tumor microenvironment cross-talk, myeloma growth induction and drug resistance, angiogenesis and signals for osteoclast activation and inhibition of osteoblasts. Additional genes induced by co-culture were exclusively deregulated in pMSCs and were predominantly associated to RNA processing, the ubiquitine-proteasome pathway, regulation of cell cycle and Wnt signaling. Primary MSCs from bone marrow (BM) samples of healthy donors (n=8) and multiple myeloma (MM) patients (n=13) were generated as described by Garayoa et al. 2009 (PMID:19357701). Ficoll-Paque density gradient separation medium was used to isolate mononuclear cells from BM aspirates. MSCs were selected by adherence to plastic and subsequently expanded until passage 2 when they were used for co-culture. For the MSC-MM.1S co-cultures we used a 6-well format transwell system with 1 M-BM-5m pore size membrane. Briefly, 2 X 10^4 MSCs were first cultured attached to the lower side of the membrane, and when reached M-bM-^IM-^H 85% confluence 1 X 10^6 MM.1S cells were seeded on the upper side. After 24 h co-culture in RPMI 1640 medium supplemented with 10% FBS and antibiotics, MSCs were recovered by trypsinization, washed once in PBS and stored at -80M-BM-0C in RLT buffer (Qiagen) until RNA extraction. Absence of MM.1S cells in the recovered MSC population was assessed in selected samples by flow cytometry analysis.
2014-11-23 | E-GEOD-46053 | biostudies-arrayexpress
Project description:Objective: An intronic GGGGCC-repeat expansion of C9ORF72 is the most common genetic variant of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. The mechanism of neurodegeneration is unknown, but a direct effect on RNA processing mediated by RNA foci transcribed from the repeat sequence has been proposed. Results: Gene level analysis revealed a number of differentially expressed networks and both cell types exhibited dysregulation of a network functionally enriched for genes encoding ‘RNA splicing’ proteins. There was a significant overlap of these genes with an independently generated list of GGGGCC-repeat protein binding partners. At the exon level, in lymphoblastoid cells derived from C9ORF72-ALS patients splicing consistency was lower than in lines derived from non-C9ORF72 ALS patients or controls; furthermore splicing consistency was lower in samples derived from patients with faster disease progression. Frequency of sense RNA foci showed a trend towards being higher in lymphoblastoid cells derived from patients with shorter survival, but there was no detectable correlation between disease severity and DNA expansion length. Significance: Up-regulation of genes encoding predicted binding partners of the C9ORF72 expansion is consistent with an attempted compensation for sequestration of these proteins. A number of studies have analysed changes in the transcriptome caused by C9ORF72 expansion, but to date findings have been inconsistent. As a potential explanation we suggest that dynamic sequestration of RNA processing proteins by RNA foci might lead to a loss of splicing consistency; indeed in our samples measurement of splicing consistency correlates with disease severity. Gene expression profiling utilised total RNA extracted from lymphoblastoid cell lines derived from human ALS patients (n=56), and controls (n=15). Thirty-one of the ALS patients had a mutation of C9ORF72.
2015-05-08 | E-GEOD-68607 | biostudies-arrayexpress
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2015-05-08 | E-GEOD-68608 | biostudies-arrayexpress
Project description:Analysis of the transcriptional profiles of mRNA and microRNA in Rasless fibroblasts. 4-Hydroxy-tamoxifen (4-OHT) treatment triggers removal of K-Ras expression in [H-Ras-/-;N-Ras-/-;K-Raslox/lox;RERTert/ert] mouse fibroblasts (named K-Raslox) generating M-bM-^@M-^\RaslessM-bM-^@M-^] MEFs which are unable to proliferate, but recover proliferative ability after ectopic expression of constitutively active downstream kinases such as BRAF and MEK1. Using Affymetrix microarrays, we compared the transcriptional profiles of Rasless fibroblasts to those of K-Raslox (MEFs lacking only H-Ras and N-Ras). We also compared the transcriptional profile of Rasless cells with those of BRAF and MEK1-transfected Rasless cells which recovered proliferative ability. Re-entry of the Rasless cells into cell cycle progression through ectopic expression of activated BRAF or MEK1 resulted in full reversion of most transcriptional alterations identified in cells lacking the three canonical Ras proteins. Pre-confluent cell cultures corresponding to the different Ras genotypes were harvested for extraction of total RNA and miRNA samples, and subsequent hybridization on Affymetrix microarrays. The different sets of experimental mRNA samples analyzed here included (i) 8 samples K-Raslox (proliferating cells expressing only K-Ras, considered as Control): 4 biological replicates, technical duplicates each; (ii) 7 samples Rasless: the same cells after treatment with 4-OHT for 12 days (to become non-proliferating fibroblasts), including 4 biological replicates and technical duplicates from 3 of them; (iii) 3 samples BRAF-rescued MEFs (Rasless cells harboring activated BRAF constructs, with regained proliferative ability): 3 biological replicates; (iv) 3 samples MEK1-rescued MEFs (Rasless cells harboring activated MEK1 constructs, with regained proliferative ability): 3 biological replicates; and their respective controls harbouring the vempty vectors (v) 2 samples Hygromycin-resistant (control for BRAF-transfected Rasless cells) including 2 biological replicates, and (vi) 4 samples Puromycin-resistant (control for MEK1-transfected Rasless cells) including 2 biological replicates, technical duplicates each. The gene expression study contains a total of 27 samples. Regarding the miRNA expression study, the experimental samples analyzed included (i) 4 samples samples K-Raslox (used as Control): 2 biological replicates, technical duplicates each; (ii) 8 samples Rasless: the same cells after treatment with 4-OHT for 6 days (2 biological replicates, technical duplicates each) and 12 days (2 biological replicates, technical duplicates each); (iii) 4 samples BRAF-rescued, including 2 biological replicates, technical duplicates each; (iv) 4 samples MEK1-rescued,including 2 biological replicates, technical duplicates each, and (v) 4 samples Puromycin-resistant empty vector, containing 2 biological replicates, technical duplicates each. The miRNA expression study contains a total of 24 samples.
2013-11-27 | E-GEOD-45222 | biostudies-arrayexpress
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2014-04-09 | E-GEOD-56615 | biostudies-arrayexpress
Project description:The role of SPROUTY2 (SPRY2) in human colon cancer is controversial. Our data support a tumorigenic action of SPRY2. We use microarrays to identify SPRY2 target genes in human SW480 ADH colon carcinoma cell line. RNA was obtained from SW480 ADH cells, Mock transfected or transfected with WT or two differents SPRY2 genes mutants. Hybridization was performed on Affymetrix microarrays. We performed three independent experiments. Each experiment was conducted in triplicate.
2016-08-01 | E-GEOD-56941 | biostudies-arrayexpress
Project description:The aim of this study consists in detecting genes regulated by N-myc in the murine cochlea In this data set we present 2688 genes differentially regulated by Nmyc in the murine cochlea. These data serve as a platform for verifying their differential regulation by N-myc via RNA in situ hybridisation or other techniques. 4 Total samples were analyzed. A pairwise comparison between two wild-type and 2 N-myc mutants samples was conducted. Genes with a FDR up to 14% are presented. Briefly, the robust microarray analysis (RMA) algorithm was used for background correction, intra- and inter-microarray normalization, and expression signal calculation. Once the absolute expression signal for each gene (i.e., the signal value for each probe set) was calculated in each microarray, a method [called significance analysis of microarray (SAM)] was applied to calculate significant differential expression and find the gene probe sets that characterized the highly metastatic samples. The method uses permutations to provide robust statistical inference of the most significant genes and provides P valuesadjusted to multiple testing using false discovery rate (FDR).
2014-09-16 | E-GEOD-61406 | biostudies-arrayexpress
Project description:Fasciolosis remains an important food-borne tremaode disease causing high morbidity around the world and affecting grazing animals and humans. A deeper understanding concerning the molecular mechanisms by which Fasciola hepatica infection occurs as well as the molecular basis involved in acquiring protection is extremely important in designing and selecting new vaccine candidates. The present study gives a first report of microarray-based technology for describing changes in splenic gene expression profile for mice immunised with a highly effective, protection-inducing,multi-epitope, subunit-based, chemically-synthesised vaccine candidate. Female CD1 mice were immunised with synthetic peptides containing B- and T-cell epitopes as novel vaccine candidates and challenged with Fasciola hepatica metacercariae. Spleen RNA from mice immunised with the highest protection-inducing synthetic peptides was isolated, amplified and labelled using Affymetrix standardised protocols. The Ingenuity Pathway Analysis tool was used to annotate bio-functions and constructing and visualising molecular interaction networks. Immunising mice with a combination of three peptides containing T-cell epitopes induced high protection against experimental challenge according to survival rates and hepatic damage scores. It also induced differential expression of 820 genes; 168 being up-regulated and 652 down-regulated. Functional study revealed changes in pathways related to nitric oxide and reactive oxygen species production, IL-12 signalling and production in macrophages and IL-8 signalling with up-regulation of S100A8, MMP9 and CXCR2 genes. The data obtained in the present study provided us with a more comprehensive overview concerning the possible molecular pathways implied in inducing protection against Fasciola hepatica in a murine model Three mice were used as healthy controls and remained untreated along the experiment. Three mice were subcutaneously immunised with our vaccine candidate on day 0, and two booster doses were applied on days 14 and 28, respectively. Two-weeks after the last immunisation, all of the mice used in the present study (including controls) were humanely euthanised by intraperitoneal injection of pentobarbital (60mg/Kg) and necropsied for spleen recovery and RNA isolation using standardised protocols. Splenic gene expression profile was compared between healthy and immunised groups.
2015-06-06 | E-GEOD-69611 | biostudies-arrayexpress
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2012-09-25 | E-GEOD-41130 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE41130: Expression profiling of Low-Risk Myelodysplastic Syndromes (MDSs) GSE41215: Methylation profiling of Low-Risk Myelodysplastic Syndromes (MDSs) Refer to individual Series
2012-09-28 | E-GEOD-41216 | biostudies-arrayexpress