This SuperSeries is composed of the SubSeries listed below.
Detailed transcriptomics analysis of the effect of dietary fatty acids on gene expression in the heart.
Sex, Treatment
View SamplesFatty acids comprise the primary energy source for the heart and are mainly taken up via hydrolysis of circulating triglyceride-rich lipoproteins. While most of the fatty acids entering the cardiomyocyte are oxidized, a small portion is involved in altering gene transcription to modulate cardiometabolic functions. So far, no in vivo model has been developed enabling study of the transcriptional effects of specific fatty acids in the intact heart. In the present study, mice were given a single oral dose of synthetic triglycerides composed of one single fatty acid. Hearts were collected 6h thereafter and used for whole genome gene expression profiling. Experiments were conducted in wild-type and PPAR/ mice to allow exploration of the specific contribution of PPAR. It was found that: 1) linolenic acid (C18:3) had the most pronounced effect on cardiac gene expression. 2) The largest similarity in gene regulation was observed between linoleic acid (C18:2) and C18:3. Large similarity was also observed between the synthetic PPAR agonist Wy14643 and docosahexaenoic acid (C22:6). 3) Many genes were regulated by one particular treatment only. Genes regulated by one particular treatment showed large functional divergence. 4) The majority of genes responding to fatty acid treatment were regulated in a PPAR-dependent manner, emphasizing the importance of PPAR in mediating transcriptional regulation by fatty acids in the heart. 5) Several genes were robustly regulated by all or many of the fatty acids studied, mostly representing well-described targets of PPARs (e.g. Acot1, Angptl4, Ucp3). 6) Deletion and activation of PPAR had a major effect on expression of numerous genes involved in metabolism and immunity. Our analysis demonstrates the marked impact of dietary fatty acids on gene regulation in the heart via PPAR.
Detailed transcriptomics analysis of the effect of dietary fatty acids on gene expression in the heart.
Sex, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.
Specimen part, Disease stage, Cell line, Subject
View SamplesMatrix induced effects on gene expression in HeLa and MDA-MB-231 cells
Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.
Cell line
View Samplesgene expression data from 3 pairs of cancer associated fibroblasts and normal fibroblasts from the same individual Overall design: mRNA seq data from 3 normal and 3 cancer associated fibroblast cell lines
Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.
Specimen part, Disease stage, Subject
View SamplesWe study the effect of nitrogen limitation on the growth and development of poplar roots. We used microarrays to detail the global program of gene expression underlying morphological and developmental changes driven by low nitrogen in the growth media. We report the effect of nitrogen limitation on the growth and development of poplar roots. Low nitrogen concentration led to increased root elongation followed by lateral root proliferation and finally increased root biomass. These morphological responses correlated with high and specific activation of genes encoding regulators of cell cycle and enzymes involved in cell wall biogenesis, growth and remodeling. Comparative analysis of poplar and Arabidopsis root transcriptomes under nitrogen deficiency indicated many similarities and diversification in the response in the two species. A reconstruction of genetic regulatory network (GRN) analysis revealed a sub-network centered on a PtaNAC1-like transcription factor. Consistent with the GRN predictions, root-specific upregulation of PtaNAC1 in transgenic poplar plants increased root biomass and led to significant changes in the expression of the connected genes specifically under low nitrogen. PtaNAC1 and its regulatory miR164 showed inverse expression profiles during response to LN, suggesting of a micro RNA mediated attenuation of PtaNAC1 transcript abundance in response to nitrogen deprivation.
Nitrogen deprivation promotes Populus root growth through global transcriptome reprogramming and activation of hierarchical genetic networks.
Specimen part, Treatment, Time
View SamplesNotch receptors direct the differentiation of T helper (Th) cell subsets, but their influence on regulatory T (TR) cell responses is obscure. Interruption of Notch signaling in TR cells resulted in a super-regulatory phenotype, with suppression of TR cell Th1 programming and apoptosis as well as Th1 cell responses in systemic inflammation. In contrast, gain of function Notch1 signaling in TR cells resulted in lymphoproliferation, dysregulated Th1 responses and autoimmunity. To determine mechanisms by which Notch signaling may alter TR cell function, we compared the transcriptional profiles of splenic TR cells of Foxp3EGFPCre mice with those of Foxp3EGFPCreR26N1c/N1c (gain of function Notch signaling), Foxp3EGFPCreRBPJ/ (loss of function canonical Notch signaling), and Foxp3EGFPCreR26N1c/N1cRBPJ/ mice (gain of function/canonical loss of function Notch signaling).
Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling.
Sex, Age, Specimen part
View SamplesFetal spleens were collected at days 82 and 97 of gestation following maternal infection with BVDV on day 75 of gestation.
Attenuated lymphocyte activation leads to the development of immunotolerance in bovine fetuses persistently infected with bovine viral diarrhea virus†.
Sex, Specimen part
View SamplesPrimary mammary gland stromal fibroblasts from pubertal SHARPIN-deficient cpdm/cpdm -mice and their littermate controls Overall design: mRNA seq data from 3 wt and 3 Sharpincpdm mouse mammary gland stromal fibroblast cell samples
SHARPIN regulates collagen architecture and ductal outgrowth in the developing mouse mammary gland.
Age, Specimen part, Cell line, Subject
View SamplesFNDC4 is a novel secreted factor sharing high homology with the exercise-associated myokine irisin (FNDC5). Here we report that Fndc4 is robustly upregulated in various mouse models of inflammation as well as in human inflammatory conditions. Specifically, subjects with inflammatory bowel disease show increased FNDC4 levels locally at inflamed sites of the intestine. Interestingly, administration of recombinant FNDC4 during colitis development in mice resulted in markedly reduced disease severity compared to mice injected with a control protein. Conversely, mice that lacked Fndc4 showed increased colitis severity. Analysis of binding of FNDC4 to different immune cell types revealed strong and specific binding to macrophages and monocytes. FNDC4 treatment of bone marrow-derived macrophages in vitro resulted in reduced phagocytosis, improved survival and reduced pro-inflammatory chemokine expression. Hence, treatment with FNDC4 resulted in a state of dampened macrophage activity, while enhancing their survival. Thus, we have characterized a novel factor with direct therapeutic potential in inflammatory bowel disease and possibly other inflammatory diseases.
FNDC4 acts as an anti-inflammatory factor on macrophages and improves colitis in mice.
Sex, Specimen part, Treatment
View Samples