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GSE77500
Mus musculus
4 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Spermatogonial 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.
Publication Title
The Luteinizing Hormone-Testosterone Pathway Regulates Mouse Spermatogonial Stem Cell Self-Renewal by Suppressing WNT5A Expression in Sertoli Cells.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 46 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Spermatogonial stem cells (SSCs) have pluripotent potential. However, frequency of pluripotent cell derivation is low and the mechanism of culture-induced reprogramming remains unknown. Here we report that epigenetic instability of germline stem (GS) cells, cultured SSCs, induces pluripotent cell derivation. GS cells undergo DNA demethylation in H19 differentially methylated region under low-density culture. When H19 demethylation was induced by Dnmt1 depletion, they converted into embryonic stem (ES)-like cells. Dnmt1 depletion downregulated Dmrt1 expression, whose depletion also induced pluripotency. Functional screening of Dmrt1 target gene revealed that Dmrt1 depletion upregulates Sox2, the key molecule responsible for generating induced pluripotent stem cells. Although Sox2 transfection upregulated Oct4 and produced pluripotent cells, this conversion was inhibited by Oct1 overexpression, suggesting that the balance of Oct proteins maintains SSC identity. These results suggest that culture-induced reprogramming is caused by unstable DNA methylation, and that Dmrt1-Sox2 cascade is critical for regulating pluripotency in SSCs.
Publication Title
Regulation of pluripotency in male germline stem cells by Dmrt1.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
A single spermatogonial stem cell can aquire pluripotentiality but that conversion into a pluripotent cell type is accompanied by loss of spermatogenic potential.
Publication Title
Pluripotency of a single spermatogonial stem cell in mice.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Expression profiling of cell cycle genes in human pancreatic islets with and without type 2 diabetes
Publication Title
Autoimmunity against INS-IGF2 protein expressed in human pancreatic islets.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The 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.
Publication Title
Molecular and genetic characterization of partial masculinization in embryonic ovaries grafted into male nude mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The onset of the liver inflamentation in the Sox17+/- embryos.
Publication Title
Sox17 haploinsufficiency results in perinatal biliary atresia and hepatitis in C57BL/6 background mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Diet-induced obesity is reported to induce a phenotypic switch in adipose tissue macrophages from an antiinflammatory M2 state to a proinflammatory M1 state. Telmisartan, an angiotensin II type 1 receptor antagonist and a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist, reportedly has beneficial effects on insulin sensitivity. We studied the effects of telmisartan on the adipose tissue macrophage phenotype in high fat-fed mice. Telmisartan was administered for 5 weeks to high fat-fed C57BL/6 mice. Insulin sensitivity, macrophage infiltration, and the gene expressions of M1 and M2 markers in epididymal fat tissues were examined. Insulin- or a glucose-tolerance test showed that telmisartan treatment improved insulin resistance, decreasing the body weight gain, visceral fat weight and adipocyte size without affecting the amount of food intake. Telmisartan treatment reduced the number of CD11c-positive cells and crown-like structures. Telmisartan reduced the mRNA expressions of M1 macrophage markers, such as TNF-alpha and IL-6, and increased the expression of M2 markers, such as IL-10 and Mgl2. The reduction of M1 macrophage markers, as well as the increased gene expression of M2 markers especially IL-10, is a possible mechanism for the improvement of insulin sensitivity by telmisartan.
Publication Title
Telmisartan improves insulin resistance and modulates adipose tissue macrophage polarization in high-fat-fed mice.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Phosphatidylcholine 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.
Publication Title
Regulatory role for phosphatidylcholine transfer protein/StarD2 in the metabolic response to peroxisome proliferator activated receptor alpha (PPARalpha).
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
In 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.
Publication Title
BD-Func: a streamlined algorithm for predicting activation and inhibition of pathways.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Resiquimod 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.
Publication Title
Modulation of the allergic asthma transcriptome following resiquimod treatment.
Sample Metadata Fields
No sample metadata fields
View Samples