This SuperSeries is composed of the SubSeries listed below.
Whole blood transcriptome analysis in amyotrophic lateral sclerosis: A biomarker study.
Sex, Disease
View SamplesTranscriptome-wide analysis of whole blood gene expression profiles of ALS patients, gender- and age-matched controls and patients diagnosed with diseases mimicking ALS at a tertiary referral center for motor neuron diseases.
Whole blood transcriptome analysis in amyotrophic lateral sclerosis: A biomarker study.
Sex, Disease
View SamplesTranscriptome-wide analysis of whole blood gene expression profiles of ALS patients, gender- and age-matched controls and patients diagnosed with diseases mimicking ALS at a tertiary referral center for motor neuron diseases.
Whole blood transcriptome analysis in amyotrophic lateral sclerosis: A biomarker study.
Sex, Disease
View SamplesBackground: It is recognized that atherosclerosis can regresses at least in animal models. However, little is known about the mechanisms. We induced regression of advanced atherosclerosis in apolipoprotein E deficient (APOE/) mice and studied underlying mechanisms. Unexpectedly, our study led to the role of interleukin-7 (IL-7) in atherogenesis.
Interleukin-7 induces recruitment of monocytes/macrophages to endothelium.
Sex, Age
View SamplesQuiescent MRC-5 fibroblasts were compared to young fibroblasts Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de) Overall design: 6 samples: 3 biological replicates for each age group: young and quiescent MRC-5 cells. 50bp, single-end reads, no strand-specific reads
Long-term quiescent fibroblast cells transit into senescence.
No sample metadata fields
View SamplesHuman fibroblasts at different population doublings were treated with low amounts of rotenone (mild stress) and compared to untreated fibroblasts. Two different cell lines were used (MRC-5, HFF). Illumina sequencing (HiSeq2000) was applied to generate 50bp single-end reads. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de) Overall design: 60 samples: 3 biological replicates for each group: MRC-5 cells at 4 different population doublings (PD) with and without rotenone; HFF cells at 6 different population doublings with and without rotenone
Hormetic effect of rotenone in primary human fibroblasts.
No sample metadata fields
View SamplesComparing gene expression level by Illumina sequencing of fibroblasts after irradiation Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de) Overall design: 6 samples, 3 samples per group, 2 groups: 1) MRC-5 cells population doublings (PD) 16 and irradiation (20GY) and 2) HFF cells PD32 and irradiation (20GY)
Conserved genes and pathways in primary human fibroblast strains undergoing replicative and radiation induced senescence.
No sample metadata fields
View SamplesSenescent human fibroblasts were compared to young proliferating fibroblasts. Five different cell lines were compared. Illumina sequencing (HiSeq2000) was applied to generate 50bp single-end reads. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de) Overall design: 48 samples: 3 biological replicates for each group: young proliferating and senescent BJ cells; young proliferating and senescent Wi-38 cells; young proliferating and senescent IMR-90 cells; 5 population doubling from young proliferating to senescent cell for HFF and MRC-5 cells
Conserved Senescence Associated Genes and Pathways in Primary Human Fibroblasts Detected by RNA-Seq.
No sample metadata fields
View SamplesER71 mutant embryos are nonviable and lack hematopoietic and endothelial lineages. To further define the functional role for ER71 in cell lineage decisions, we generated genetically modified mouse models. We engineered an ER71-EYFP transgenic mouse model by fusing the 3.9 kb ER71 promoter to the EYFP reporter gene. Using FACS and transcriptional profiling, we examined the EYFP+ populations of cells in ER71 mutant and wildtype littermates. In the absence of ER71, we observed an increase in the number of EYFP expressing cells, increased expression of the cardiac molecular program and decreased expression of the hemato-endothelial program compared to the wildtype littermate controls. We have also generated a novel ER71-Cre transgenic mouse model using the same 3.9 kb ER71 promoter. Genetic fate mapping studies revealed that the ER71 expressing cells daughter hematopoietic and endothelial lineages in the wildtype background. In the absence of ER71, these cell populations contributed to alternative mesodermal lineages including the cardiac lineage. To extend these analyses, we used an inducible ES/EB system and observed that ER71 overexpression repressed cardiogenesis. Together, these studies identify ER71 as a critical regulator of mesodermal fate decisions, acting to specify the hematopoietic and endothelial lineages at the expense of cardiac lineages. This enhances our understanding of the mechanisms that govern mesodermal fate decisions early during embryogenesis.
ER71 directs mesodermal fate decisions during embryogenesis.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Temporal- and strain-specific host microRNA molecular signatures associated with swine-origin H1N1 and avian-origin H7N7 influenza A virus infection.
Cell line
View Samples