LRAT knockout mice on vitamin A sufficient or deficient diets were compared to age-matched wildtype mice on a vitamin A sufficient diet
Effects of vitamin A deficiency in the postnatal mouse heart: role of hepatic retinoid stores.
Sex, Specimen part
View SamplesLRAT knockout mice on vitamin A sufficient or deficient diets were compared to age and gender matched wildtype mice on a vitamin A sufficient diet
Effects of vitamin A deficiency in the postnatal mouse heart: role of hepatic retinoid stores.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Effects of vitamin A deficiency in the postnatal mouse heart: role of hepatic retinoid stores.
Sex, Specimen part
View SamplesMurine MafB/c-MAF double KO (Maf-DKO) primary macrophages are known for their unlimited non-tumorigenic self-renewal ability (Aziz et al., 2009). In an in vitro screen for cytokines and small molecules we identified Niacinamide (NAM) a potent inhibitor of their proliferative potential characterized by a reversible cell cycle arrest.
SIRT1 regulates macrophage self-renewal.
Specimen part
View SamplesGPR68 is an essential flow sensor in arteriolar endothelium, and is a critical signaling component in cardiovascular pathophysiology Overall design: RNAseq of cells from mesenteric endothelium of mice plus and minus GPR68
GPR68 Senses Flow and Is Essential for Vascular Physiology.
Specimen part, Cell line, Treatment, Subject
View SamplesMyocardial infarction (MI) is one of the most severe manifestations of coronary artery disease (CAD) and the leading cause of death from non-infectious diseases worldwide. It is known, that the central component of CAD pathogenesis is a chronic vascular inflammation. However, the mechanisms underlying the changes that occur in T, B and NK-lymphocytes, monocytes and other immune cells during CAD and MI are still poorly understood. One of those pathogenic mechanisms might be the dysregulation of intracellular signaling pathways in the immune cells.
Collapsing the list of myocardial infarction-related differentially expressed genes into a diagnostic signature.
Sex, Specimen part, Disease stage
View SamplesChromosomal instability (CIN) is defined by the propensity to acquire structural and/or numerical aberration in the normal cellular karyotype and is often associated with cancer. Autophagy is a catabolic process that leads to the recycling of cellular components that may positively or negatively impact on cancer development and progression, depending on the context. Recent work postulated that the depletion of the pro-autophagic and tumor suppressive protein Beclin 1 triggers CIN by interfering with mitotic chromosome segregation, providing a possible mechanism for how Beclin 1 can act as a tumor suppressor (Fremont et al., PMID: 23478334). Here, we present data supporting the notion that the phenotypes described in Fremont et al., depend on a siRNA off-target effect. The transcriptomic analysis shown here was designed to identify the factor(s) that are responsible for such phenotype.
Beclin 1 is dispensable for chromosome congression and proper outer kinetochore assembly.
Cell line
View SamplesThis series represents isolated alveolar macrophages from human subjects.
A distinctive alveolar macrophage activation state induced by cigarette smoking.
No sample metadata fields
View SamplesMotivation: Sample source, procurement process, and other technical variations introduce batch effects into genomics data. Algorithms to remove these artifacts enhance differences between known biological covariates, but also carry potential concern of removing intra-group biological heterogeneity and thus any personalized genomic signatures. As a result, accurate identification of novel subtypes from batch corrected genomics data is challenging using standard algorithms designed to remove batch effects for class comparison analyses. Nor can batch effects be corrected reliably in future applications of genomics-based clinical tests, in which the biological groups are by definition unknown a priori.
Preserving biological heterogeneity with a permuted surrogate variable analysis for genomics batch correction.
Sex, Specimen part, Disease, Disease stage, Race
View SamplesIn the central nervous system (CNS), the microRNAs (miRNAs), small endogenous RNAs exerting a negative post-transcriptional regulation on mRNAs, are involved in major functions, such as neurogenesis, and synaptic plasticity. Moreover, they are essential to define the specific transcriptome of the tissues and cell types. However, few studies were performed to determine the miRNome of the different structures of the rat CNS, even through rat is a major model in neuroscience. We determined the miRNome profile of the hippocampus, the cortex, the striatum, the spinal cord and the olfactory bulb, by small RNA-Seq. We found a total of 365 known miRNAs' and 90 novel miRNAs expressed in the CNS of the rat. Novel miRNAs seemed to be important in defining structure-specific miRNomes. Differential analysis showed that several miRNAs were specifically enriched/depleted in these CNS structures. Then, we correlated miRNAs' expression with the expression of their mRNA targets by mRNA-Seq. This analysis suggests that the transcriptomic identity of each structure is regulated by specific miRNAs. Altogether, these results suggest the critical role played by these enriched/depleted miRNAs in the functional identities of CNS structures. Overall design: miRNA and mRNA profile of 5 structures of the central nervous system of rat, for each structurewe analyzed three biological replicates
Small RNA-Seq reveals novel miRNAs shaping the transcriptomic identity of rat brain structures.
Specimen part, Cell line, Subject
View Samples