Project description:Prior to generation of microarray data for a Top-down Systems analysis of influenza A infection, we evaluated the degree and origin of technical variation in gene expression microarray data from mouse lungs and compared this to inter-animal variation. Technical variation in these microarray data in the context of inter-animal variation supported a choice of biological rather than technical replicates. A) One mouse (260) was infected with 0.6LD50 of the mouse pathogenic H1N1 strain PR8. Lung tissues were collected at 72h post infection and processed to yield whole lung RNA that was used for microarray analysis. The RNA was extracted in 3 individual batches (I, II, III), each batch of RNA was amplified in 2 separate batches (1,2), and the individual batches of amplified product were again hybridized in 2 batches. This dataset contains 18 microarrays covering 1 experimental condition with 1 biological replicate and a matrix of technical replicates. B) 3 mice (245, 246, 247) were infected with 0.6LD50 of the mouse pathogenic H1N1 strain PR8. Lung tissues were collected at 72h post infection and processed to yield whole lung RNA that was used for microarray analysis. From each animal, RNA was extracted, the RNA was amplified in three separate batches (A, B, C), and the individual batches of amplified product were again hybridized in 2 batches. This dataset contains 24 microarrays covering 1 experimental condition with 3 biological replicates and a matrix of technical replicates. Datasets A) and B) are linked to two biological datasets - one comparing the transcriptomes of 5 different cell types isolated from individual lungs of influenza A-infected or control animals (contains 75 microarrays covering 25 experimental conditions) and one comprising whole lung microarrays from sham-infected or influenza H1N1-infected animals (contains 138 microarrays, 19 experimental conditions, 7 biological replicates).

2013-07-03 | E-GEOD-42521 | biostudies-arrayexpress

Transcriptomic profiling of lung endothelial cells at different stages of lung colonization by MDA-MB-231-LM2 cells

Project description:In cancer progression to metastasis, disseminated cancer cells frequently lodge near vasculature in secondary organs. However, our understanding of the cellular crosstalk evoked at perivascular sites is still rudimentary. In this study, we identified an inter-cellular machinery governing formation of a pro-metastatic vascular niche during breast cancer colonization in lungs. Transcriptomic analysis of endothelial cells (ECs) isolated from mouse lungs with metastases revealed a marked upregulation of genes linked to proliferation, inflammation and numerous secreted proteins. We showed that four secreted factors, INHBB, SCGB3A1, OPG and LAMA1, induced in ECs form a supportive niche that promotes metastasis in mice, by enhancing stem cell properties and survival ability of cancer cells. Interestingly, the blocking vascular endothelial cell growth factor (VEGF), a major cytokine regulating EC behaviors, dramatically suppressed EC proliferation whereas no impact was observed on the expression of the four vascular niche factors in lung ECs. We found that the formation of a vascular niche is correlated with inflammation, and revealed that metastasis-associated macrophages are essential for production of all of four niche factors in lung ECs. Macrophages are activated via TNC-TLR4 at perivasculature and sequentially stimulate ECs to produce the four niche factors. Thus, our findings provide mechanistic insights into the formation of a perivascular niche and offer the possibility that targeting macrophages may synergize with existing anti-angiogenic drugs to effectively suppress vascular function in metastatic colonization. We used microarrays to analyze the global changes of gene expression in lung endothelial cells at different stages of lung colonization by MDA-MB-231-LM2 cells

2021-12-31 | GSE156349 | GEO

Metastasis-initiating cells induce and exploit a fibroblast niche to fuel malignant colonization of the lungs.

Project description:Metastatic colonization relies on interactions between disseminated cancer cells and the microenvironment in secondary organs. Here, we show that disseminated breast cancer cells evoke phenotypic changes in lung fibroblasts, forming a supportive metastatic niche. Colonization of the lungs confers an inflammatory phenotype in metastasis-associated fibroblasts. Specifically, IL-1α and IL-1β secreted by breast cancer cells induce CXCL9 and CXCL10 production in lung fibroblasts via NF-κB signaling, fueling the growth of lung metastases. Notably, we find that the chemokine receptor CXCR3, that binds CXCL9/10, is specifically expressed in a small subset of breast cancer cells, which exhibits tumor-initiating ability when co-transplanted with fibroblasts and has high JNK signaling that drives IL-1α/β expression. Importantly, disruption of the intercellular JNK-IL-1-CXCL9/10-CXCR3 axis reduces metastatic colonization in xenograft and syngeneic mouse models. These data mechanistically demonstrate an essential role for the molecular crosstalk between breast cancer cells and their fibroblast niche in the progression of metastasis.

| S-EPMC7083860 | biostudies-literature

Mesenchymal cancer cell-stromal crosstalk promotes niche activation, epithelial reversion and metastatic colonization

Project description:The experiment was design to address the intrinsic differences between metastatic cancer stem cells in the primary tumour and during metastatic colonization in the mouse mammary gland tumour model MMTV-pyMT. Total RNA was prepared from the indicated cancer cells freshly isolated, stained and FACS sorted either from primary tumours or from lungs upon intravenous injection of cancer cells.

2015-11-21 | E-GEOD-63558 | biostudies-arrayexpress

Epigenetic modules governing skin epidermal homeostasis

Project description:Epigenetic modules governing skin epidermal homeostasis

| PRJNA808412 | ENA

garlic inter-root soil

Project description:garlic inter-root soil Raw sequence reads

| PRJNA1085538 | ENA

Inter-layer and inter-subject variability of circadian gene expression in human skin

Project description:Inter-layer and inter-subject variability of circadian gene expression in human skin

| PRJNA844020 | ENA

Epigenetic modules governing skin epidermal homeostasis [III]

Project description:Epigenetic modules governing skin epidermal homeostasis [III]