{"owner": "ArrayExpress Uploader", "pop_total": 0, "id": 1455, "factors": [{"GSE3920GSM89650": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon gamma"}}, {"GSE3920GSM89652": {"CELLTYPE": "fibroblast", "COMPOUND": "interferon alpha"}}, {"GSE3920GSM89642": {"CELLTYPE": "endothelial cell", "COMPOUND": "control"}}, {"GSE3920GSM89647": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon alpha"}}, {"GSE3920GSM89654": {"CELLTYPE": "fibroblast", "COMPOUND": "control"}}, {"GSE3920GSM89647": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon alpha"}}, {"GSE3920GSM89647": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon alpha"}}, {"GSE3920GSM89647": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon alpha"}}, {"GSE3920GSM89642": {"CELLTYPE": "endothelial cell", "COMPOUND": "control"}}, {"GSE3920GSM89654": {"CELLTYPE": "fibroblast", "COMPOUND": "control"}}, {"GSE3920GSM89658": {"CELLTYPE": "fibroblast", "COMPOUND": "interferon gamma"}}, {"GSE3920GSM89650": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon gamma"}}, {"GSE3920GSM89642": {"CELLTYPE": "endothelial cell", "COMPOUND": "control"}}, {"GSE3920GSM89641": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon beta"}}, {"GSE3920GSM89642": {"CELLTYPE": "endothelial cell", "COMPOUND": "control"}}, {"GSE3920GSM89654": {"CELLTYPE": "fibroblast", "COMPOUND": "control"}}, {"GSE3920GSM89658": {"CELLTYPE": "fibroblast", "COMPOUND": "interferon gamma"}}, {"GSE3920GSM89647": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon alpha"}}, {"GSE3920GSM89650": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon gamma"}}, {"GSE3920GSM89652": {"CELLTYPE": "fibroblast", "COMPOUND": "interferon alpha"}}, {"GSE3920GSM89641": {"CELLTYPE": "endothelial cell", "COMPOUND": "interferon beta"}}, {"GSE3920GSM89652": {"CELLTYPE": "fibroblast", "COMPOUND": "interferon alpha"}}, {"GSE3920GSM89642": {"CELLTYPE": "endothelial cell", "COMPOUND": "control"}}], "ownerprofile_id": "arrayexpress_sid", "platform": 3, "summary_wrapped": "IFNs are highly pleiotropic cytokines also endowed with marked anti-angiogenic activity. In this study, the mRNA expression profiles of...", "pubmed_id": 17202376, "geo_gse_id": "E-GEOD-3920", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 2, "sample_count": 23, "tags": ["cell", "chemokine", "protein"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_gds_id": "", "slug": "transcription-profiling-of-human-endothelial-and-f", "geo_id_plat": "E-GEOD-3920_A-AFFY-33", "name": "Transcription profiling of human endothelial and fibroblast cells isolated from umbilical cord veins treated with interferons to identify genes regulated by interferons", "created": "Jun.19, 2014", "summary": "IFNs are highly pleiotropic cytokines also endowed with marked anti-angiogenic activity. In this study, the mRNA expression profiles of endothelial cells (EC) exposed in vitro to IFN-alpha, IFN-beta, or; IFN-gamma were determined. We found that in HUVEC as well as in other EC types 175 genes were upregulated (>2-fold increase) by IFNs, including genes involved in the host response to RNA viruses, inflammation, and apoptosis. Interestingly, 41 genes showed a >5-fold higher induction by IFN-alpha in EC compared to human fibroblasts; among them, the gene encoding the angiostatic chemokine CXCL11 was selectively induced by IFN-alpha in EC along with other genes associated; with angiogenesis regulation, including CXCL10, TRAIL, and guanylate binding protein 1 (GBP-1). These transcriptional changes were confirmed and extended by quantitative PCR analysis and ELISA; whereas IFN-alpha and IFN-beta exerted virtually identical effects on transcriptome modulation, a differential gene regulation by type I and type II IFN emerged, especially as far as quantitative aspects were concerned. In vivo, IFN-alpha-producing tumors over-expressed murine CXCL10-11,; GBP-1 and TRAIL, with evidence of CXCL11 production by tumor-associated EC. Overall, these findings improve our understanding of the anti-angiogenic effects of IFNs by showing that these cytokines trigger an anti-angiogenic transcriptional program in EC. Moreover, we suggest that quantitative differences in the magnitude of the transcriptional activation of IFNresponsive genes could form the basis for cell-specific transcriptional signatures. In press, J. Immunol. 2007. Experiment Overall Design: comparison of interferon effects on endothelial cells (HUVEC, HMVEC) and fibrobloasts", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-3920", "species": "human", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-3920/samples/"}