This SuperSeries is composed of the SubSeries listed below.
Genome-wide DNA methylation analysis of articular chondrocytes reveals a cluster of osteoarthritic patients.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesThe aim of this study is to identify, for the first time, the genome-wide DNA methylation profiles of human articular chondrocytes from OA and healtly cartilage samples.
Genome-wide DNA methylation analysis of articular chondrocytes reveals a cluster of osteoarthritic patients.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesPrevious results from a genome scan in a F2 Iberian by Meishan intercross showed several chromosome regions associated with litter size traits. In order to identify candidate genes underlying these QTL we have performed an ovary gene expression analysis during pregnancy. F2 sows were ranked by their estimated breeding values for prolificacy, the six sows with higher EBV (HIGH prolificacy) and the six with lower EBV (LOW prolificacy) were selected. Samples were hybridized to Affymetrix porcine expression microarrays. The statistical analysis with a mixed-model approach identified 221 differentially expressed probes, representing 189 genes. These genes were functionally annotated in order to identify the genetic pathways overrepresented. Among the most represented functional groups the first one was immune system response activation against external stimulus. The second group was made up of genes which regulate the maternal homeostasis by complement and coagulation cascades. The last group was involved on lipid and fatty acid enzymes of metabolic processes, which participate in steroidogenesis pathway. In order to identify powerful candidate genes for prolificacy, the second approach of this study was merging microarray data with position information of QTL affecting litter size, previously detected in the same experimental cross. According to this, we have identified 27 differentially expressed genes co-localized with QTL for litter size traits, which fulfill the biological, positional and functional criteria.
Differential gene expression in ovaries of pregnant pigs with high and low prolificacy levels and identification of candidate genes for litter size.
Specimen part
View SamplesThe aim of this study was to identify differences in the NK-cell response towards Leishmania mexicana lipophosphoglycan (LPG) between patients with localized (LCL) and diffuse (DCL) cutaneous leishmaniasis through gene expression profiling, in an attempt to pinpoint alterations in the signaling pathways responsible for the NK-cell dysfunction in patients with DCL.
Down-Regulation of TLR and JAK/STAT Pathway Genes Is Associated with Diffuse Cutaneous Leishmaniasis: A Gene Expression Analysis in NK Cells from Patients Infected with Leishmania mexicana.
Specimen part, Disease, Disease stage, Treatment
View SamplesIdentification of genes and causal mutations regulating growth and fatness traits in pig. Overall design: Transcriptome sequencing of 10 liver samples of two groups of divergent pigs for growth and fatness.
Using RNA-Seq SNP data to reveal potential causal mutations related to pig production traits and RNA editing.
Sex, Age, Specimen part, Subject
View SamplesWe studied the influence of the oleic acid content of the diet on adipose tissue transcriptome.
Dietary energy source largely affects tissue fatty acid composition but has minor influence on gene transcription in Iberian pigs.
Sex, Specimen part, Treatment
View SamplesWe studied the influence of genetic type (pure Iberian pigs vs crossbred with Duroc) on l.dorsi transcriptome
Longissimus dorsi transcriptome analysis of purebred and crossbred Iberian pigs differing in muscle characteristics.
Sex, Age, Specimen part
View SamplesTransriptional profiling of white adipose tissue extracted from obese mice.
Loss of mitochondrial protease OMA1 alters processing of the GTPase OPA1 and causes obesity and defective thermogenesis in mice.
Age, Specimen part
View SamplesBackground & Aims. Glycine N-methyltransferase (GNMT) is an essential regulator of the total transmethylation flux in the mammalian liver. Distinct DNA methylation patterns are characteristic of liver development, hepatic de-differentiation and liver disease progression, processes in which the levels of GNMT decrease dramatically by mechanisms still poorly understood. Interestingly, putative binding sites for the microRNA miRNA-873-5p were identified in the 3´UTR of GNMT suggesting a potential role for miRNA-873-5p in GNMT regulation. Results. We have identified that the hepatic expression of miRNA-873-5p was increased in a cohort of cirrhotic and liver cancer patients associated with a down-regulation of GNMT levels. Moreover, during liver development, hepatic de-differentiation and fibrosis, the elevation of miRNA-873-5p coincided with the reduction of GNMT expression, indicating that miRNA-873-5p specifically targets the expression of GNMT. Under these circumstances, inhibition of miRNA-873-5p induced GNMT levels and decreased global CpG methylation and transmethylation flux. Indeed, reestablishment of GNMT expression by miRNA-873-5p inhibition reduced hepatocyte de-differentiation, and abolished completely the mortality produced after bile duct ligation as a result of decreased proinflamatory and profibrogenic markers. miRNA-873-5p knockdown-mediated antifibrotic effect was significantly blunted if its effect on GNMT was blocked. Conclusion. Taken together, our studies highlight the role of miRNA-873-5p as a key regulator of GNMT expression, paving the way for new therapeutical approaches in liver de-differentiation and fibrosis. Overall design: Genome-wide changes in gene Expression in mouse livers from BDL treated or not with anti-miR-873 were generated by RNAseq.
MiR-873-5p acts as an epigenetic regulator in early stages of liver fibrosis and cirrhosis.
Age, Cell line, Treatment, Subject
View SamplesThe identification of inflammatory bowel disease (IBD) susceptibility genes by genome-wide association has linked this pathology to autophagy, a lysosomal degradation pathway that is crucial for cell and tissue homeostasis. Here, we describe autophagin-1 (ATG4B) as an essential protein in the control of inflammatory response during experimental colitis. In this pathological condition, ATG4B protein levels increase paralleling the induction of autophagy. Moreover, ATG4B expression is significantly reduced in affected areas of the colon from IBD patients. Consistently, atg4b-/- mice present Paneth cell abnormalities, as well as an increased susceptibility to DSS-induced colitis. Atg4b-deficient mice exhibit significant alterations in proinflammatory cytokines and mediators of the immune response to bacterial infections, which are reminiscent of those found in patients with Crohns disease or ulcerative colitis. Additionally, antibiotic treatments and bone marrow transplantation from wild-type mice reduced colitis in atg4b-/- mice. Taken together, these results provide additional evidence on the importance of autophagy in intestinal pathologies and describe ATG4B as a novel protective protein in inflammatory colitis. Finally, we propose that Atg4b-null mice are a suitable model for in vivo studies aimed at testing new therapeutic strategies for intestinal diseases associated with autophagy deficiency
ATG4B/autophagin-1 regulates intestinal homeostasis and protects mice from experimental colitis.
Sex, Age, Specimen part, Treatment
View Samples