Lactoferrin is a highly multifunctional protein. Indeed, it is involved in many physiological functions, including regulation of iron absorption and immune responses.
A nutritional supplement containing lactoferrin stimulates the immune system, extends lifespan, and reduces amyloid <i>β</i> peptide toxicity in <i>Caenorhabditis elegans</i>.
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View SamplesCocoa protein content is a very interesting source for isolation of antioxidant bio-peptides, which can be used for the prevention of age-related diseases. We use microarrays to study the global genome expression of C. elegans fed with a peptide (13L) isolated from cocoa.
A cocoa peptide protects Caenorhabditis elegans from oxidative stress and β-amyloid peptide toxicity.
No sample metadata fields
View SamplesNumerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabditis elegans as host. C. elegans were fed on different LAB strains (78 in total) and nematode viability was assessed after oxidative stress (3mM and 5mM H2O2). One strain, identified as Lactobacillus rhamnosus CNCM I-3690, protected worms by increasing their viability by 30% and, also, increased average worm lifespan by 20%. We performed a transcriptomic analysis of C. elegans fed with this strain and showed that increased lifespan is correlated with differential expression of the DAF-16/insulin-like pathway, which is highly conserved in humans.
Anti-inflammatory Lactobacillus rhamnosus CNCM I-3690 strain protects against oxidative stress and increases lifespan in Caenorhabditis elegans.
Time
View SamplesThe pathogenic mechanisms of common kidney glomerular diseases, including the vast majority of cases of proteinuria, remain unknown.
Glomerular transcriptome changes associated with lipopolysaccharide-induced proteinuria.
No sample metadata fields
View SamplesThe activation of vascular smooth muscle cells (VSMCs) during hypertension-induced arterial remodeling processes relies on a change of the gene expression program, i.e., up-regulation of genes to induce migration, proliferation and matrix degradation/synthesis. At the same time, genes controlling the quiescent, contractile VSMC phenotype are down-regulated. We used microarrays to detail the global program of gene expression underlying hypertension-induced vascular remodeling in the presence and absence of regulator of G-protein signaling 5 (RGS5) and identified distinct classes of down-regulated genes during vascular remodeling when RGS5 was not present.
Hypertension-evoked RhoA activity in vascular smooth muscle cells requires RGS5.
Sex, Specimen part, Treatment
View SamplesPurpose:To take a comprehensive effort in characterizing the brain vasculature gene expression upon hyperglycemia. Methods: We extracted mRNA from brain microvasculature fragments isolated from a genetic mouse model of hyperglycemia (Ins2-AKITA) and WT mice and analyzed their transcriptome with RNA sequencing The samples were sequenced on an Illumina HiSeq 2500 sequencer at the SNP&SEQ sequencing facility (Science for Life laboratory (SciLifeLab), Uppsala sequencing node). The reads were aligned to the Ensembl mouse gene assembly (NCBIM37) using Tophat2 software (version 2.0.4). The duplicated reads were removed using the picard tool (version 1.92). To identify the genes significantly enriched in the pericyte samples as compared with microvascular samples, statistical tests were performed using the Cufflinks tool (version 2.2.1) Results: Twenty-three genes were significantly regulated in mutant when compared to WT (False Discovery Rate < 0.05) Overall design: The microvascular RNA from two male heterozygous Ins2-AKITA mice and three littermate wild-type controls were processed and sequenced on the Illumina HiSeq 2500 platform in the sequencing facility in Uppsala University.
Prolonged systemic hyperglycemia does not cause pericyte loss and permeability at the mouse blood-brain barrier.
Sex, Specimen part, Subject
View SamplesLittle is known about the pan-microvascular transcriptome, particularly considering gene transcripts and their encoded proteins that can be considered as vascular-selective in their expression.
Identification of a core set of 58 gene transcripts with broad and specific expression in the microvasculature.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma.
Specimen part, Treatment
View SamplesSince direct pharmacological inhibition of RAS has thus far been unsuccessful, we explored system biology approaches to identify synergistic drug combination(s) that can mimic direct RAS inhibition. Leveraging an inducible mouse model of NRAS-mutant melanoma, we compare pharmacological MEK inhibition to complete NRAS-Q61K extinction in vivo. NRAS-Q61K extinction leads to a complete and durable tumor regression by enhancing both apoptosis and cell cycle arrest. By contrast, MEK inhibition only produces tumor stasis at best and we find that it robustly activates apoptosis but does not significantly impede proliferation.
Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma.
Specimen part
View SamplesWe sought to understand the pathways involved in NRAS extinction over time using a doxycycline-dependent, inducible mouse model of melanoma. This data provides insights into the temporal dynamics of downstream NRAS signaling and helps to correlate differentially affected pathways.
Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma.
Specimen part, Treatment
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