While the survival rate of HIV-infected individuals has dramatically improved with the development of highly active anti-retroviral therapy, HIV-infected individuals have an increased risk for chronic disorders, including the development of COPD, manifesting as emphysema. The mechanisms of HIV-associated emphysema are not understood. Based on the knowledge that human airway basal cells (BC) function as stem/progenitor cells capable of differentiation into specialized ciliated and secretory cells during natural turnover and repair in response to injury, we hypothesized that HIV interacts with, and consequently induces pathologic programming of the BC that contributes to the development of emphysema. Overall design: Studies were designed to assess: (1) if HIV binds to, infects and/or replicates in BC; (2) identify which BC receptor(s) are responsible for HIV capture; and (3) the reprogramming of BC biology upon HIV exposure. Infectious HIVNL4-3 was used for all studies. Soluble heparan sulfate and heparinase III were used to prevent HIV/BC interactions. BC phenotypes after HIV exposure were assessed by TaqMan quantitative PCR, ELISA, phospho-MAPK array, protease array, cell invasion assay, and zymography.
HIV Reprograms Human Airway Basal Stem/Progenitor Cells to Acquire a Tissue-Destructive Phenotype.
Specimen part, Disease, Disease stage, Subject
View SamplesGene expression profiling of primary mouse articular chondrocyte infected with recombinant adenovirus expressing the zinc transporter ZIP8 (SLC39A8) protein.
Pleiotropic roles of metallothioneins as regulators of chondrocyte apoptosis and catabolic and anabolic pathways during osteoarthritis pathogenesis.
Age, Specimen part, Treatment
View SamplesThe Drosophila phagocytic receptor Eater is expressed specifically in phagocytic hemocytes. It contributes to host immune defense and is required for survival of bacterial infections. Eater is involved in recognition and phagocytosis of bacteria.
Phagocytosis of bacterial pathogens.
Cell line, Treatment, Time
View SamplesAnalysis between two different types of T cells
Comparison of Invariant NKT Cells with Conventional T Cells by Using Gene Set Enrichment Analysis (GSEA).
Sex, Specimen part
View SamplesComparative analysis of mouse cardiac left ventricle gene expression: voluntary wheel exercise and pregnancy-induced cardiac hypertrophy
Distinct cardiac transcriptional profiles defining pregnancy and exercise.
Sex, Specimen part
View SamplesThe placenta is an understudied organ that has a critical role in mammalian development. In early placental development, the essential process of trophoblast invasion establishes adequate blood flow between mother and fetus. Despite its importance, little is known about the genomic regions responsible for regulating trophoblast invasion. In order to identify enhancers that are important for regulating the process, we carried out ChIP-Seq for an enhancer-associated mark at two time points during early placental development. Combining these data with RNA-Seq data and protein interaction data allowed us to construct a gene-enhancer network describing trophoblast invasion. Overall design: RNA-Seq at two time points in early placenta development (e7.5 an e9.5). There are 3 biological replicates per time point. Samples were pooled and sequenced on two lanes.
Changes in the enhancer landscape during early placental development uncover a trophoblast invasion gene-enhancer network.
No sample metadata fields
View SamplesAbstract: The Drosophila trachea is a branched tubular epithelia that transports oxygen and other gases. trachealess (trh), which encodes a bHLH-PAS transcription factor, is among the first genes to be expressed in the cells that will form the trachea. In the absence of trh, tracheal cells fail to invaginate to form tubes and remain on the embryo surface. Expression of many tracheal-specific genes depends on trh, but all of the known targets have relatively minor phenotypes compared to loss of trh, suggesting that there are additional targets. To identify uncharacterized transcriptional targets of Trh and to further understand the role of Trh in embryonic tracheal formation, we performed an in situ hybridization screen using a library of ~100 tracheal-expressed genes identified by the Berkeley Drosophila Genome Project (BDGP). Surprisingly, expression of every tracheal gene we tested was dependent on Trh, suggesting a major role for Trh in activation and maintenance of tracheal gene expression. A re-examination of the interdependence of the known early-expressed transcription factors, including trh, ventral veinless (vvl) and knirps/knirps-related (kni/knrl), suggests a new model for how gene expression is controlled in the trachea, with trh regulating expression of vvl and kni, but not vice versa. A pilot screen for the targets of Vvl and Kni/Knrl revealed that Vvl and Kni have only minor roles compared to Trh. Finally, genome-wide microarray experiments identified additional Trh targets and revealed that a of biological processes are affected by the loss of trh.
Trachealess (Trh) regulates all tracheal genes during Drosophila embryogenesis.
No sample metadata fields
View SamplesmRNA expression profiles for 3 breast cancer cell lines seeded at different density and grown for different duration Overall design: This experiment is part of a study fo the effect of cell density on drug sensitivity [1]. Cells plated at different densities in 384-well plates were harvested at the indicated times and RNA was extracted using the RNeasy mini kit (Qiagen). To ensure sufficient RNA amounts wells with low cell numbers were pooled. Some conditions have been tested in biollogical replicates grown at the same time. Libraries were prepared by the Broad Technology Labs (BTL) following the protocol for SCRB-Seq described in [2]. Transcripts were quantified by the BTL computational pipeline using Cuffquant version 2.2.1 [3]. [1] Hafner, M., Niepel, M., Chung, M., Sorger, P.K., Growth rate inhibition metrics correct for confounders in measuring sensitivity to cancer drugs. DOI:10.1038/NMETH.3853 [2] Soumillon, M., Cacchiarelli, D., Semrau, S., van Oudenaarden, A. & Mikkelsen, T.S. Characterization of directed differentiation by high-throughput single-cell RNA-Seq http://biorxiv.org/content/early/2014/03/05/003236 [3] Trapnell, C., Roberts, A., Goff, L., Pertea, G., Kim, D., Kelley, D.R., Pimentel, H., Salzberg, S.L., Rinn, J.L. & Pachter, L. Differential gene and transcript expression analysis of RNA-seq experiments with TopHat and Cufflinks, Nat. Protoc. 7, 562-578 (2012).
Growth rate inhibition metrics correct for confounders in measuring sensitivity to cancer drugs.
Subject
View SamplesIn the present study, to identify potential paracrine factor for the stromal regulation of E2-induced epithelial cell proliferation, we treated epithelial and stromal cell populations of mouse uterine primary co-culture with either oil or E2. Three independent RNA pools prepared for each population were then subjected to the Affymetrix gene chip analysis for the whole mouse genome transcripts. Our data revealed up-regulation of 119 genes and down-regulation of 28 genes in epithelial cell populations and up-regulation of 144 genes and down-regulation of 192 genes in stromal cell population.
Estrogen mediated epithelial proliferation in the uterus is directed by stromal Fgf10 and Bmp8a.
Specimen part, Treatment
View SamplesMfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfngs roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown altered Notch activation, decreased tumor sphere formation in vitro, and reduced tumor growth in xenograft model. To identify the potential downstream targets of Mfng during CLBC tumorigenesis, we compared the gene expression profiles between xenografts tumor derived from of MDA-MB231 cells carrying Mfng shRNA and the control vector. Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfngs roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown caused alteration in Notch activation, associated with decreased tumor sphere formation in vitro, as well as reduced tumor growth in xenograft model. We intend to compare gene expression profiles between xenografts of MDA-MB231 cells carrying Mfng shRNA and the control vector. This project seeks to identify potential downstream targets of Mfng in CLBC.
Manic fringe promotes a claudin-low breast cancer phenotype through notch-mediated PIK3CG induction.
Specimen part, Treatment
View Samples