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SRP064621
Mus musculus
4 Downloadable Samples
Illumina HiSeq 2000
Description
The alveolar type 1 (AT1) cell covers >95% of the gas exchange surface and is extremely thin to facilitate passive gas diffusion. The development of this highly specialized cell is poorly understood including fundamental questions regarding cell number and morphology. Using new molecular stereology and single cell imaging methods, we show that AT1 cells develop via a non-proliferative two-step process while maintaining proliferative potential. In the flattening step, AT1 cells remodel cell junctions and undergo molecular specification. In the folding step, AT1 cells are sculptured to match secondary septa formation, resulting in a single AT1 cell spanning multiple alveoli. AT1 cells grow in size by >10-fold, fueling most of the postnatal lung growth. Strikingly AT1 cells proliferate upon ectopic SOX2 expression and undergo stage-dependent cell fate reprogramming. These results contradict the traditional view of AT1 cells being terminally differentiated and provide insights to alveolar maturation. In this experiment, we conducted next-generation sequencing on flow-sorter AT1 cells isolated from mouse lungs ectopically expressing Sox2 under the control of the AT1-specific promoter Scnn1a versus control AT1 cells. Overall design: Two samples of Sox2-expressing AT1 cells versus two control AT1 samples.
Publication Title
The development and plasticity of alveolar type 1 cells.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Multiple Myeloma (MM) is an hematological malignancy. MM cells are resistant to X-ray irradiations. We irradiated RPMI 8226 cancer cells with C-ions, which are more energetic than X-ray irradiations. We found that MM cells, RPMI 8226, are also resistant to C-ion irradiations.
Publication Title
HIF-1α and rapamycin act as gerosuppressant in multiple myeloma cells upon genotoxic stress.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
A549 cells were grown at air liquid interphase (ALI) and exposed to airborne formaldehyde for three days. An exposure platform was developed for this purpose, which provided the volatile analyte in a humidified atmosphere. The platform was composed of a reference and an exposure chamber.
Publication Title
Cellular reactions to long-term volatile organic compound (VOC) exposures.
Sample Metadata Fields
Cell line
View Samples- Mus musculus, Rattus norvegicus
- 43 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
BET bromodomains mediate transcriptional pause release in heart failure.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 23 Downloadable Samples
Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Heart failure (HF) is driven via interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. While pathologic gene transactivation in this context is known to be associated with recruitment of histone acetyl-transferases and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in HF. Using a chemical genetic approach, we establish a central role for BET-family bromodomain proteins in gene control during HF pathogenesis. BET inhibition potently suppresses cardiomyocyte hypertrophy in vitro and pathologic cardiac remodeling in vivo. Integrative transcriptional and epigenomic analyses reveal that BET proteins function mechanistically as pause-release factors critical to activation of canonical master regulators and effectors that are central to HF pathogenesis and relevant to the pathobiology of failing human hearts. This study implicates epigenetic readers in cardiac biology and identifies BET co-activator proteins as therapeutic targets in HF.
Publication Title
BET bromodomains mediate transcriptional pause release in heart failure.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 20 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Heart failure (HF) is driven via interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. While pathologic gene transactivation in this context is known to be associated with recruitment of histone acetyl-transferases and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in HF. Using a chemical genetic approach, we establish a central role for BET-family bromodomain proteins in gene control during HF pathogenesis. BET inhibition potently suppresses cardiomyocyte hypertrophy in vitro and pathologic cardiac remodeling in vivo. Integrative transcriptional and epigenomic analyses reveal that BET proteins function mechanistically as pause-release factors critical to activation of canonical master regulators and effectors that are central to HF pathogenesis and relevant to the pathobiology of failing human hearts. This study implicates epigenetic readers in cardiac biology and identifies BET co-activator proteins as therapeutic targets in HF.
Publication Title
BET bromodomains mediate transcriptional pause release in heart failure.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 30 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Human umbilical cord Whartons jelly stem cells (WHJSC) are gaining attention as a possible clinical source of mesenchymal stem cells for use in cell therapy and tissue engineering due to their high accessibility, expansion potential and plasticity. However, the cell viability changes that are associated to sequential cell passage of these cells are not known. In this analysis, we have identified the gene expression changes that are associated to cell passage in WHJSC.
Publication Title
Evaluation of the cell viability of human Wharton's jelly stem cells for use in cell therapy.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The objective of this study was to analyze gene expression associated to extracellular matrix components of normal palmar fascia and tissues affected by Dupuytren's disease.
Publication Title
Identification of histological patterns in clinically affected and unaffected palm regions in dupuytren's disease.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 74 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Vitamin D deficiency has been associated with increased esophageal cancer risk. Vitamin D controls many downstream regulators of cellular processes including proliferation, apoptosis, and differentiation. We evaluated the effects of vitamin D supplementation on global gene expression in patients with Barrett's esophagus.
Publication Title
A nonrandomized trial of vitamin D supplementation for Barrett's esophagus.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Upon antigen recognition within peripheral lymphoid organs, B cells interact with T cells and other immune cells to transiently form morphological structures called germinal centers (GCs), which are required for B cells clonal expansion, immunoglobulin class switching, and affinity maturation. This process, known as the GC response, is an energetically demanding process that requires metabolic reprogramming of B cells. Here, we showed that the Ras-related guanosine triphosphate hydrolase (GTPase) R-Ras2 (also known as TC21) plays an essential, nonredundant, and B cellintrinsic role in the GC response. Both the conversion of B cells into GC B cells and their expansion were impaired in mice lacking R-Ras2, but not in those lacking a highly-related R-Ras subfamily member or both the classic H-Ras and N-Ras GTPases. In the absence of R-Ras2, activated B cells did not increase oxidative phosphorylation or aerobic glycolysis. We showed that R-Ras2 was an effector of both the B cell receptor (BCR) and CD40 and that, in its absence, B cells exhibited impaired activation of the PI3K-Akt-mTORC1 pathway, reduced mitochondrial DNA replication, and decreased expression of genes involved in glucose metabolism. Because most human B cell lymphomas originate from GC B cells or B cells that have undergone the GC response, our data suggests that R-Ras2 may also regulate metabolism in B cell malignancies.
Publication Title
R-Ras2 is required for germinal center formation to aid B cells during energetically demanding processes.
Sample Metadata Fields
Specimen part
View Samples