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E-GEOD-2638

ABSTRACT: Transcription profiling by array of human mammary epithelial cells (HMEC) stimulated with TNF vs. controls reveals TNF induces distinct expression programs

OTHER RELATED OMICS DATASETS IN: PRJNA92283PRJNA92281

PROVIDER: E-GEOD-2638 | ExpressionAtlas | 2014-08-15

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-2638-analysis-methods.tsv	Tabular
	E-GEOD-2638-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-2638-configuration.xml	Xml
	E-GEOD-2638-percentile-ranks.tsv	Tabular
	E-GEOD-2638.condensed-sdrf.tsv	Tabular

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E-GEOD-2639

Project description:Transcription profiling by array of human umbilical vein endothelial cells (HUVEC) stimulated with TNF vs. controls reveals TNF induces distinct expression programs

2014-08-15 | E-GEOD-2639 | ExpressionAtlas

CXCL10 promotes vascular permeability upon TNF-induced release from pericytes

Project description:Tumor necrosis factor alpha induces vascular permeability, playing an important role in inflammation. Also, TNF-induced vascular leakage is involved in the increased extravasation of nanoparticle formulated chemotherapeutics improving drug delivery and subsequently tumor response, and we found a positive correlation between the presence of pericytes in the tumor-associated vasculature and TNF-induced leakage. RNA sequencing and pathway analysis of TNF-stimulated versus non-stimulated pericytes and endothelial cells show significant upregulation of several pathways involving interferon regulating pathways with a high expression of CXCL10, also known as Interferon gamma-inducible protein 10 (IP-10) in TNF-stimulated pericytes. In addition, CXCL10 protein production was significantly increased in conditioned medium from TNF-exposed pericytes compared to the other conditions. In our animal studies, we observed that tumor types with high pericyte covered vessels show enhanced permeability when exposed to TNF, which can be blocked with a neutralizing CXCL10 antibody. Vice versa, tumors with vessels low in pericyte number do not respond to TNF, i.e., do not express elevated permeability. Importantly, this lack of pericyte coverage can be compensated by co-administration of CXCL10. Our finding reveals a mechanism where TNF induces CXCL10 release from pericytes, being at the basis of increased permeability and thus vascular leakage.

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RNA-seq of two human mammary epithelial cell lines (HMLE and HMLE-Twist-ER) treated with 4-hydroxytamoxifen vs control

Project description:Immortalized non-cancerous human mammary epithelial cells (HMLE) were transfected to express the murine fusion protein Twist1-estrogen receptor(point mutation G525R) (HTER). Twist1-mediated gene expression is activated by stimulation with 4-hydroxytamoxifen for several days and induces an epithelial-mesenchymal transition (EMT) in HTER cells. In breast cancer, EMT equips cancer cells for metastasis and therapy resistance. As control, HTER cells were treated with vehicle (methanol). As additional controls, HMLE cells were stimulated with 4-hydroxytamoxifen or methanol, respectively. Prior to RNA sequencing, EMT-undergoing HTER cells were sorted by fluorescence-activated cell sorting (FACS) based on E-Cadherin and CD44 surface protein levels into three populations, epithelial (E), hybrid epithelial-mesenchymal (EM), and mesenchymal (M): E-Cadherin_high_CD44_low (E), E-Cadherin_medium_CD44_medium (EM), and E-Cadherin_low_CD44_high (M).

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Proteomic and phosphoproteomic profiling of human myoepithelial and luminal epithelial cells

Project description:The aim of the project is to perform deep proteomic and phosphoproteomic profiling of luminal epithelial and myoepithelial cells from the mammary gland of young vs. older women.

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PU.1 and C/EBPalpha synergistically program distinct response to NF-kappaB activation through establishing monocyte specific enhancers (expression data)

Project description:Unraveling the complexity of transcriptional programs coded by different cell types has been one of the central goals of cell biology. Using genome-wide location analysis, we examined how two different cell types generate different responses to the NF-kappaB signaling pathway. We showed that, after tumor necrosis factor-alpha (TNF-alpha) treatment, NF-kappaB p65 subunit binds to distinct genome locations and subsequently induces different subsets of genes in human monocytic THP-1 cells versus HeLa cells . Interestingly, the differential p65 binding in two cell types correlates with pre-existing cell-type specific enhancers prior to TNF-alpha stimulation, marked by histone modifications. We also found that two transcription factors, PU.1 and C/EBPalpha, appear to synergistically mediate enhancer creation and affect NF-kappaB target selection in THP-1 cells. In HeLa cells, co-expression of PU.1 and C/EBPalpha conferred TNF-alpha responsiveness to a subset of THP-1 specific NF-kappaB target genes. These results suggest that the diversity of transcriptional programs in mammalian cells arises, at least in part, from pre-existing enhancers that are established by cell specific transcription factors. We used Affymetrix microarray (GPL570) to obtain gene expression data for THP1 and HeLa cells before and after TNF-alpha treatment.

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Bovine mammary epithelial cells in response to artemisinin treatment

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