Expression profiling by array
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE56490 | GEO | 2014/12/31
SECONDARY ACCESSION(S): PRJNA243488
REPOSITORIES: GEO
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Project description:Human keratinocytes isolated from foreskin were cultured and treated with a GSK-3beta inhibitor, BIO. The effect of BIO was evaluated by the cell growth, clony formation and differentiating markers. We used microarrays to detail the global program of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.
2011-02-24 | GSE27509 | GEO
Project description:Human keratinocytes isolated from foreskin were cultured and treated with a GSK-3beta inhibitor, BIO. The effect of BIO was evaluated by the cell growth, clony formation and differentiating markers. We used microarrays to detail the global program of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Human primary keratinocytes were subjected for RNA extraction. The total RNAs were hybridized on Affymetrix microarrays. The cultured cells exhibit a homogous cell morphology at passage 1 to passage 5. The cells were treated with BIO at passage 3 or 4.
2011-02-24 | E-GEOD-27509 | biostudies-arrayexpress
Project description:This study examines patterns of genome-wide transcriptional response to the active form of vitamin D, 1,25-dihyroxyvitamin D3 (1,25D), and the bacterial lipopolysaccharide (LPS) in primary human monocytes, to better understand pathways underlying the immunomodulatory role of 1,25D. Total RNA extraced from monocytes from 20 healthy individuals of African-African and European-American ancestry treated with 1,25D alone or in the presence of LPS for 24 hours.
2016-02-20 | E-GEOD-78083 | biostudies-arrayexpress
Project description:Vitamin D is the strongest known natural anti-proliferative. A large number of studies in a wide spectrum of cancers, including epidemiological, in vitro and animal models, demonstrate that the active form of Vitamin D has anti-cancer benefits, affecting both progression and metastasis. Alike the role in calcium Vitamin D regulation, its anti-proliferative effect is thought to function through the Vitamin D receptor (VDR), although convincing evidence is lacking. Notwithstanding, separation of the calcemic and the anti-proliferative activity of Vitamin D analogues has been a major obstacle in developing new drugs for the treatment of cancer. The work presented attempts to unveil the molecular mechanism behind the anti-proliferative action of Vitamin D using genomic tools. For that purpose four independently developed Vitamin D sensitive/resistant MCF7 cell line pairs were collected. These unique biological replicates enabled us, both to increase the power of our study and to omit the use of Vitamin D. We deem this omission crucial since in the presence of Vitamin D only downstream genes involved in proliferation and cell cycle would be identified rather than causal resistance genes. The use of a variety of genomic techniques including expression, NMD and oligo CGH arrays reveal in the resistant cell lines the 11q13-14 as a region of DNA copy number loss and an altered expression of EGFR signaling pathway genes. Surprisingly, no genes known from calcium Vitamin D regulation were identified, nor did the VDR silencing by RNAi induce resistance to the sensitive cell lines. Keywords: comparative genomic hybridization, cell type comparision
2008-06-01 | GSE9887 | GEO
Project description:CD14+ human monocytes differentiating into DCs in the presence of IL4 and GM-CSF were treated with agonists for RXR and its partners or vehicle 18 hours after plating (experiment with RXR and permissive partners, donor 1-3) or 14 hours after plating (experiment with nonpermissive partners, donor 4-6). Cells were harvested 12 hours thereafter. Experiments were performed in biological triplicates representing samples from three different donors. In this study all probable RXR-signaling pathways induced by agonists for RXR, LXRs, PPARs, RAR and VDR were identified in differentiating human monocyte-derived dendritic cells.
2010-09-01 | GSE23073 | GEO
Project description:We have carried out global gene expression analysis to clarify the interrelationship between 1,25-dihydroxyvitamin D3 and differentiation-driven gene expression patterns in developing human monocyte-derived dendritic cells. Monocytes were treated with 10 nM 1,25-dihydroxyvitamin D3 or vehicle 14 hours after plating for 12 hours or 5 days. Monocytes, differentiating dendritic cells (+/-1,25-dihydroxyvitamin D3 for 12 hours) and immature dendritic cells (+/-1,25-dihydroxyvitamin D3 for 5 days) were harvested. This design allows one to identify genes regulated by differentiation and/or 1,25-dihydroxyvitamin D3 in human monocyte-derived dendritic cells. Experiment Overall Design: Human monocytes were obtained from buffy coats from healthy donors by Ficoll gradient centrifugation followed by immunomagnetic cell separation with anti-CD14-conjugated microbeads. Monocytes were cultured in RPMI-1640 supplemented with 10% FBS, 800 U/ml GM-CSF and 500 U/ml IL-4. Monocytes were treated with 10 nM 1,25-dihydroxyvitamin D3 or vehicle 14 hours after plating for 12 hours or 5 days. Monocytes, differentiating dendritic cells (+/-1,25-dihydroxyvitamin D3 for 12 hours) and immature dendritic cells (+/-1,25-dihydroxyvitamin D3 for 5 days) were harvested. Experiments were performed in biological triplicates representing samples from different donors. 15 samples were processed and hybridized to Human Genome U133 Plus 2.0 Arrays.
2009-02-21 | E-GEOD-13762 | biostudies-arrayexpress
Project description:Vitamin D is the strongest known natural anti-proliferative. A large number of studies in a wide spectrum of cancers, including epidemiological, in vitro and animal models, demonstrate that the active form of Vitamin D has anti-cancer benefits, affecting both progression and metastasis. Alike the role in calcium Vitamin D regulation, its anti-proliferative effect is thought to function through the Vitamin D receptor (VDR), although convincing evidence is lacking. Notwithstanding, separation of the calcemic and the anti-proliferative activity of Vitamin D analogues has been a major obstacle in developing new drugs for the treatment of cancer. The work presented attempts to unveil the molecular mechanism behind the anti-proliferative action of Vitamin D using genomic tools. For that purpose four independently developed Vitamin D sensitive/resistant MCF7 cell line pairs were collected. These unique biological replicates enabled us, both to increase the power of our study and to omit the use of Vitamin D. We deem this omission crucial since in the presence of Vitamin D only downstream genes involved in proliferation and cell cycle would be identified rather than causal resistance genes. The use of a variety of genomic techniques including expression, NMD and oligo CGH arrays reveal in the resistant cell lines the 11q13-14 as a region of DNA copy number loss and an altered expression of EGFR signaling pathway genes. Surprisingly, no genes known from calcium Vitamin D regulation were identified, nor did the VDR silencing by RNAi induce resistance to the sensitive cell lines. Keywords: comparative genomic hybridization, cell type comparision Several MCF7 breast tumor cell lines independently derived from the human breast cancer cell line, both resistant and sensitive to Vitamin D, were used. The pairs of cell lines (parental-resistant) were developed in different laboratories and using different methodologies; while some cell lines acquired resistance by long exposure to the physiological concentration of Vitamin D (100nM), others were induced to resistant by being exposed to increasing amounts of Vitamin D. A total of 4 microarray expression experiments were carried out. In all microarray experiments DNA from the Vitamin D resistant cell line was hybrizided agains DNA from the respsective sensitive/parental cell line.
2008-05-31 | E-GEOD-9887 | biostudies-arrayexpress
Project description:A role for vitamin A in host defense against Mycobacterium tuberculosis has been suggested through epidemiological and in vitro studies; however, the antimicrobial mechanism is unclear. Here, we demonstrate that vitamin A mediates host defense through regulation of cellular cholesterol content. Comparison of monocytes stimulated with all-trans retinoic acid (ATRA) or 1,25-dihydroxyvitamin D3, the biologically active forms of vitamin A and vitamin D respectively, indicates that ATRA and 1,25D3 induce mechanistically distinct antimicrobial activities. Gene expression profiling reveals that ATRA but not 1,25D3 triggers a lipid metabolism and efflux pathway, including expression of lysosomal lipid transport gene NPC2. ATRA-induced decrease in total cellular cholesterol content, subcellular lipid reorganization, lysosomal acidification and antimicrobial activity are all dependent upon expression of NPC2. Finally, the addition of HIV-protease inhibitors known to inhibit cholesterol efflux, Ritonavir and Nelfinavir, blocked both ATRA-induced cholesterol decrease as well as antimicrobial activity. Taken together, these results suggest that the vitamin A-mediated host defense mechanism against M. tuberculosis requires regulation of cellular cholesterol. Monocytes derived from four independent healthy blood donors that were stimulated with control (CTRL), ATRA or 1,25D3 at 10-8M for 18 hours.
2013-12-31 | E-GEOD-46268 | biostudies-arrayexpress
Project description:This study examines patterns of genome-wide transcriptional response to the active form of vitamin D, 1,25-dihyroxyvitamin D3 (1,25D), and the bacterial lipopolysaccharide (LPS) in primary human monocytes, to better understand pathways underlying the immunomodulatory role of 1,25D.
2016-02-20 | GSE78083 | GEO
Project description:To analyze the transcriptome changes of differentiating monocytes in response to type I IFNs, RNA seq was performed. The MACS-purified mouse BM monocytes were cultured in the presence or absence of I IFNs for 12 h or 24h under the condition of M-CSF, samples were harvested for total RNAs and subjected to RNA sequencing analyses.
2022-12-31 | GSE192418 | GEO