Background: Marketing products with added-value characteristics is a current trend in livestock production systems. Regarding meat, selection for intramuscular fat and muscular fatty acid composition is a way to improve the palatability and juiciness of meat while assuring a healthy fat content. This represents selecting animal with a different muscular metabolic profile with respect to the extended selection of lean animals. Results: The present study has analysed the muscular gene expression profiles of 68 commercial Duroc pigs belonging to two groups with extreme phenotypes for traits strongly related with lipid deposition and composition. This has allowed us to compare the physiological and metabolic implications of selecting for each of these extreme groups. Rather than upregulation of a single pathway, the main differences lied on the transcriptional levels of genes related with lipogenesis and lipolysis, revealing the existence of a cycle where triacylglycerols are continuously synthesized and degraded. Most strikingly, several genes which enhanced fatty acid -oxidation and favoured insulin signalling and glucose uptake were upregulated in the fattest animals, indicating that the events leading to peripheral insulin resistance in humans with increased levels of intramuscular fat and obesity do not take place in these pigs. Moreover, neither was detected the well-characterised low-grade inflammatory state observed in overweighed humans. Conclusion: As a whole, our data suggest that selection for increasing intramuscular fat content in pigs would lead to a shift but not a disruption of the metabolic homeostasis of muscle cells. Future studies on the post-translational changes affecting protein activity or expression as well as information about protein location within the cell would be needed to fully understand how lipid deposition affects muscle physiology in pigs.
Muscle transcriptomic profiles in pigs with divergent phenotypes for fatness traits.
Age, Specimen part
View SamplesPatients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in individuals with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (p<0.0001) were found to be up-regulated in platelets from SLE patients as compared to healthy volunteers. Notably, patients with a history of vascular disease had increased expression of type I IFN-regulated proteins as well as more activated platelets as compared with patients without vascular disease. We suggest that interferogenic immune complexes stimulate production of IFN which up-regulates the megakaryocytic type I IFN-regulated genes and proteins. This could affect platelet activation and contribute to development of vascular disease in SLE. In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE.
Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease.
Sex, Age, Specimen part, Disease
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Sumoylation coordinates the repression of inflammatory and anti-viral gene-expression programs during innate sensing.
Specimen part
View SamplesBone marrow derived dendritic cells were generated from Ubc9[fl;-] and Ubc9[+/+] mice. After in vitro derivation in the presence of GM-CSF, dendritic cells were treated with tamoxifen for four days to cause CreERT2 activation, and induce Ubc9 floxed allele deletion. This allowed comparative transcriptomic analysis of Ubc9[+/+] and Ubc9[-/-] dendritic cells unstimulated or stimulated with 10ng/ml LPS for one hour and six hours.
Sumoylation coordinates the repression of inflammatory and anti-viral gene-expression programs during innate sensing.
Specimen part
View SamplesThe expression profiles of 64 neuroblastic tumors (mainly neuroblastoma) were determined on Affymetrix chips HG U133 Plus 2.0.
Somatic and germline activating mutations of the ALK kinase receptor in neuroblastoma.
No sample metadata fields
View SamplesThe expression profiles of five human trunk level neural crest cell lines were determined on Affymetrix chips HG U133 Plus 2.0.
Epistasis between RET and BBS mutations modulates enteric innervation and causes syndromic Hirschsprung disease.
Sex, Specimen part
View SamplesLiver RNA was collected from three genotypes: WT controls, KCP knockout (KCP-KO) mutants, and KCP-Transgenic (KCP-Tg) overexpressing mice.
The kielin/chordin-like protein KCP attenuates nonalcoholic fatty liver disease in mice.
Specimen part
View SamplesClassically activated (M1) macrophages protect from infection but can cause inflammatory disease and tissue damage while alternatively activated (M2) macrophages reduce inflammation and promote tissue repair. Modulation of macrophage phenotype may be therapeutically beneficial and requires further understanding of the molecular programs that control macrophage differentiation. A potential mechanism by which macrophages differentiate may be through microRNA (miRNA), which bind to messenger RNA and post-transcriptionally modify gene expression, cell phenotype and function. The inflammation-associated miRNA, miR-155, was rapidly up-regulated over 100-fold in M1, but not M2, macrophages. Inflammatory M1 genes and proteins iNOS, IL-1b and TNF-a were reduced up to 72% in miR-155 knockout mouse macrophages, but miR-155 deficiency did not affect expression of genes associated with M2 macrophages (e.g., Arginase-1). Additionally, a miR-155 oligonucleotide inhibitor efficiently suppressed iNOS and TNF-a gene expression in wild-type M1 macrophages. Comparative transcriptional profiling of unactivated (M0) and M1 macrophages derived from wild-type and miR-155 knockout (KO) mice revealed an M1 signature of approximately 1300 genes, half of which were dependent on miR-155. Real-Time PCR of independent datasets validated miR-155's contribution to induction of iNOS, IL-1b, TNF-a, IL-6 and IL-12, as well as suppression of miR-155 targets Inpp5d, Tspan14, Ptprj and Mafb. Overall, these data indicate that miR-155 plays an essential role in driving the differentiation and effector potential of inflammatory M1 macrophages.
Control of the Inflammatory Macrophage Transcriptional Signature by miR-155.
Specimen part, Treatment
View SamplesA new method to measure elongation and intitiation rates Overall design: Reversal inhibition of transcription with DRB and tagging newly transcribed RNA with 4-thiouridine (4sU)
4sUDRB-seq: measuring genomewide transcriptional elongation rates and initiation frequencies within cells.
No sample metadata fields
View SamplesThe activation profiles of macrophages under different immune and inflammatory conditions have generated great interest. LPS, in particular, is a commonly used in vitro model of infection and inflammation studies in macrophages. We have used gene expression microarrays to define the effects of each of three variables; LPS dose, LPS vs. interferons beta and gamma, and genetic background on the transcriptional response of mouse bone marrow-derived macrophages
Analysis of the transcriptional networks underpinning the activation of murine macrophages by inflammatory mediators.
No sample metadata fields
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