Gene expression analysis to compare control cells and sorted cells
Identification of two major autoantigens negatively regulating endothelial activation in Takayasu arteritis.
Specimen part
View SamplesThe accumulation of intramyocellular lipid (IMCL) is recognized as an important determinant of insulin resistance, and is increased by a high-fat diet (HFD). However, the effects of HFD on IMCL and insulin sensitivity are highly variable.
Increased intramyocellular lipid/impaired insulin sensitivity is associated with altered lipid metabolic genes in muscle of high responders to a high-fat diet.
Sex, Specimen part, Time
View SamplesThe fetal ovarian grafts under the kidney capsule of adult male mice undergo a partial sex-reversal showing ectopic SOX9-positive Sertoli cell-like cells around 15-20 days post-transplantation. However, the molecular bases of such masculinization of fetal ovaries in the paternal environment were unclear.
Molecular and genetic characterization of partial masculinization in embryonic ovaries grafted into male nude mice.
Specimen part
View SamplesThe onset of the liver inflamentation in the Sox17+/- embryos.
Sox17 haploinsufficiency results in perinatal biliary atresia and hepatitis in C57BL/6 background mice.
Specimen part
View SamplesPhosphatidylcholine transfer protein (PC-TP, a.k.a StarD2) is abundantly expressed in liver and is regulated by PPAR. When fed the synthetic PPAR ligand fenofibrate, Pctp-/- mice exhibited altered lipid and glucose homeostasis. Microarray profiling of liver from fenofibrate fed wild type and Pctp-/- mice revealed differential expression of a broad array of metabolic genes, as well as their regulatory transcription factors. Because its expression controlled the transcriptional activities of both PPAR and HNF4 in cell culture, the broader impact of PC-TP on nutrient metabolism is most likely secondary to its role in fatty acid metabolism.
Regulatory role for phosphatidylcholine transfer protein/StarD2 in the metabolic response to peroxisome proliferator activated receptor alpha (PPARalpha).
Sex, Age, Specimen part
View SamplesIn order to validate the utility of a novel pathway algorithm (BD-Func), we test if an LBH589 signature based data from 3 cell lines (GSE36509) in an independent experiment in vivo.
BD-Func: a streamlined algorithm for predicting activation and inhibition of pathways.
Specimen part, Treatment
View SamplesSpermatogonial stem cells (SSCs) provide foundation for spermatogenesis by undergoing continuous self-renewal division. Previous studies have reported conflicting results on the role of the pituitary gland activity in SSC self-renewal. In this study, we analyzed the role of hormonal regulation of SSCs using Lhcgr (luteinizing hormone/choriogonadotropin receptor) knockout mice. Analysis of gene expression profiles showed that testes of Lhcgr-deficient mice exhibit significantly enhanced Wnt5a expression in Sertoli cells.
The Luteinizing Hormone-Testosterone Pathway Regulates Mouse Spermatogonial Stem Cell Self-Renewal by Suppressing WNT5A Expression in Sertoli Cells.
Sex, Specimen part
View SamplesResiquimod is a nucleoside analog belonging to the imidazoquinoline family of compounds which is known to signal through Toll-like receptor 7. Resiquimod treatment has been demonstrated to inhibit the development of allergen induced asthma in experimental models. Despite this demonstrated effectiveness, little is known about the molecular events responsible for this effect. The aim of the present study was to elucidate the molecular processes which were altered following resiquimod treatment and antigen challenge in a mouse model of allergic asthma. Employing microarray analysis, we have characterized the asthmatic transcriptome of the murine lung and determined that it includes genes involved in: the control of cell cycle progression, airway remodelling, the complement and coagulation cascades, and chemokine signalling. We have demonstrated that systemic resiquimod administration resulted in the recruitment of NK cells to the lungs of the mice, although no causal relationship between NK cell recruitment and treatment efficacy was found. Furthermore, results of our studies demonstrated that resiquimod treatment resulted in the normalization of the expression of genes involved with airway remodelling and chemokine signalling, and in the modulation of the expression of genes including cytokines and chemokines, adhesion molecules, and B-cell related genes, involved in several aspects of immune function and antigen presentation. Overall, our findings identified several genes, important in the development of asthma pathology, that were normalized following resiquimod treatment thus improving our understanding of the molecular consequences of resiquimod treatment in the lung milieu.
Modulation of the allergic asthma transcriptome following resiquimod treatment.
No sample metadata fields
View SamplesWT vs. Spp1-/- MPPs showed distict patterns in tgene transcription profiles when analyzed with single cell sequencing Overall design: MPPs from mice treated with thioglycollate were FACS-sorted, and gene expression profiles were compared between WT vs. Spp1-/- cells.
Skewing of the population balance of lymphoid and myeloid cells by secreted and intracellular osteopontin.
Subject
View SamplesEwings sarcoma is highly malignant bone tumor that involves childhood and adolescent, and its nature has not been well understood. To clarify its cellular origin and the mechanisms of tumorigenesis, we used ex vivo approach to create a murine model for Ewings sarcoma. The osteochondrogenic progenitors derived from the embryonic superficial zone (eSZ, designated as FZ in the data set) of murine long bones at late gestation were purified by microdissection, introduced with EWS-FLI1 or EWS-ERG retroviruses and transplanted into nude mice. Ewings sarcoma-like small round cell sarcoma developed at 100% penetrance, whereas tumor induction was less effective when growth place (GP)-derived cells were used. The different response of gene expression to EWS-FLI1 between eSZ and GP cells suggests importance of the specific cellular context for EWS-FLI1 to induce Ewings sarcoma. The Wnt/-catenin pathway was involved in close relationship to the cellular context, with Dkk2 and Wipf1 as important downstream modulators. Furthermore, gene expression profiling revealed similarity between our models and human Ewings sarcoma. These results indicate that Ewings sarcoma originates from the embryonic osteochondrogenic progenitor.
Ewing's sarcoma precursors are highly enriched in embryonic osteochondrogenic progenitors.
Specimen part, Time
View Samples