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accession-icon GSE38093
Diet-Induced Obesity Exacerbates Inflammatory and Oxidative Stress Responses in Mice Exposed to Cigarette Smoke
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To identify biosignatures that describe these lifestyle susceptibility factors, we performed parallel exposures of regular weight (RW) C57BL/6 and diet-induced obese (DIO) C57BL/6 mice to cigarette smoke, either mainstream (MS) or sidestream (SS), mimicking both the smoker and environmental exposure through second-hand smoke, respectively.

Publication Title

Impaired transcriptional response of the murine heart to cigarette smoke in the setting of high fat diet and obesity.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE47022
Impaired Transcriptional Response of the Murine Heart To Cigarette Smoke in the Setting of High Fat Diet and Obesity
  • organism-icon Mus musculus
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To identify biosignatures that describe these lifestyle susceptibility factors, we performed parallel exposures of regular weight (RW) C57BL/6 and diet-induced obese (DIO) C57BL/6 mice to cigarette smoke, either mainstream (MS) or sidestream (SS), mimicking both the smoker and environmental exposure through second-hand smoke, respectively.

Publication Title

Impaired transcriptional response of the murine heart to cigarette smoke in the setting of high fat diet and obesity.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE38092
Diet-Induced Obesity Reprograms the Inflammatory Response of the Murine Lung to Inhaled Endotoxin
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To identify key biological pathways that define susceptibility factors for pulmonary infection during obesity, diet-induced obese (DIO) and regular weight (RW) C57BL/6 mice were exposed to 0.5 g/L inhaled lipopolysaccharide (LPS) for 1 hr/d for 4 days over a period of 2 weeks.

Publication Title

Diet-induced obesity reprograms the inflammatory response of the murine lung to inhaled endotoxin.

Sample Metadata Fields

Specimen part

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accession-icon GSE75693
Mining the Human Urine Proteome for Monitoring Renal Transplant Injury
  • organism-icon Homo sapiens
  • sample-icon 76 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression data was analyzed to map with urine proteomics data

Publication Title

Mining the human urine proteome for monitoring renal transplant injury.

Sample Metadata Fields

Specimen part

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accession-icon GSE50994
Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Silymarin (SM) is a popular botanical medicine with purported liver protective effects. SM displays multiple effects in animal models and in cell culture including prevention of liver disease, reduction of inflammation, oxidative stress, and proliferation. Despite a plethora of data indicating that SM impinges on multiple cellular signaling pathways important in inflammation and disease, no unifying mechanisms have been forwarded. To define how SM elicits so many biological effects, the current study presents the first comprehensive transcriptional profiling study of human hepatoma cells treated with SM. The intention of the study was to focus on the early transcriptional events that are associated with SM-induced inhibition of proliferation and inflammation. Collectively, the data demonstrate that SM causes a rapid transcriptional reprogramming of cells that initially manifests as energy stress and slowing of cellular metabolism, leading to inhibition of cell growth and inflammation.

Publication Title

Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Time

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accession-icon SRP094977
RNA-seq in neutrophils from Juvenile Idiopathic Arthritis
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

In this study, we explored transcriptional complexity in human neutrophils from juvenile idiopathis arthritis and healthy control. We obtained differentially expressed genes among 3 ADU (active disease, untreated), 3 ADT (active disease, treated) and 2 HC (healthy control) samples using Cuffdiff2 software. Overall design: 3 ADU (active disease, untreated), 3 ADT (active disease, treated) and 2 HC (healthy control) samples were carried out RNA-Seq by next-generation sequencing strategy

Publication Title

Chromatin landscapes and genetic risk for juvenile idiopathic arthritis.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP043525
Extensive crosstalk between lncRNAs and mRNAs in mouse stem cells
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To determine the temporal variation of mRNA levels, we collected and sequenced poly-adenylated RNA from all cell extracts, cytoplasmic and nuclear fractions of a conditional Dicer mutant [DTCM23/49 XY (Nesterova et al. 2008)] mouse Embryonic Stem Cells before induction of Dicer excision (day 0) and at days 4, 8, 10 and 12 following Dicer loss of function. coverage. Overall design: RNA from whole cell extracts was collected at days 0, 4, 8, 10 and 12 following loss of Dicer function and from the cytoplasmic and nuclear fractions of cell at day 0 and 12. Three biological replicates were obtained for all samples. Poly-adenylated directional 100 base paired-end sequencing libraries were prepared for all extracts and sequenced by BGI solutions (Hong Kong).

Publication Title

Extensive microRNA-mediated crosstalk between lncRNAs and mRNAs in mouse embryonic stem cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP162342
RNA-Seq of LRRK2 G2019S Parkinson's iPSC-derived astrocytes
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Non-neuronal cell types such as astrocytes can contribute to Parkinson's disease (PD) pathology. The G2019S mutation in leucine-rich repeat kinase 2 (LRRK2) is one of the most common known causes of familial PD. To characterize its effect on astrocytes, we developed a protocol to produce midbrain-patterned astrocytes from human induced pluripotent stem cells (iPSCs) derived from PD LRRK2 G2019S patients and healthy controls. In order to understand the effect of this mutation on astrocyte function, we compared the gene expression profiles of iPSC-derived midbrain-patterned astrocytes from PD patients with those from healthy controls. Overall design: Bulk RNA-Seq profiles of human iPSC-derived midbrain-patterned astrocytes from 7 donors, including 4 patients with Parkinson's disease who carry the LRRK2 G2019S mutation, and 3 healthy control individuals

Publication Title

RNA sequencing reveals MMP2 and TGFB1 downregulation in LRRK2 G2019S Parkinson's iPSC-derived astrocytes.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon SRP094473
A neural basis for melanocortin-4 receptor-regulated appetite.
  • organism-icon Mus musculus
  • sample-icon 63 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Pro-opiomelanocortin (POMC)- and agouti-related peptide (AgRP)-expressing neurons of the arcuate nucleus of the hypothalamus (ARC) are oppositely regulated by caloric depletion and coordinately stimulate and inhibit homeostatic satiety, respectively. This bimodality is principally underscored by the antagonistic actions of these ligands at downstream melanocortin-4 receptors (MC4R) in the paraventricular nucleus of the hypothalamus (PVH). Although this population is critical to energy balance, the underlying neural circuitry remains unknown. Using mice expressing Cre recombinase in MC4R neurons, we demonstrate bidirectional control of feeding following real-time activation and inhibition of PVH(MC4R) neurons and further identify these cells as a functional exponent of ARC(AgRP) neuron-driven hunger. Moreover, we reveal this function to be mediated by a PVH(MC4R)?lateral parabrachial nucleus (LPBN) pathway. Activation of this circuit encodes positive valence, but only in calorically depleted mice. Thus, the satiating and appetitive nature of PVH(MC4R)?LPBN neurons supports the principles of drive reduction and highlights this circuit as a promising target for antiobesity drug development. Overall design: Single-neuron mRNA-seq was performed on fluorescently-labeled or -unlabeled cells that were manually isolated from dissociated adult mouse paraventricular and arcuate hypothalamus: Mc4r-2a-Cre::L10-GFP+ or Mc4r-2a-Cre::AAV-XFP+ or Mc4r-2a-Cre::AAV-XFP-negative PVH neurons; Agrp-IRES-Cre::L10-GFP+ ARC neurons; Pomc-hrGFP+ ARC neurons; and vGLUT2-IRES-Cre::AAV-XFP+ ARC neurons Note: Raw files unavailable for samples GSM2413312 GSM2413313 GSM2413314 GSM2413346 GSM2413347

Publication Title

A neural basis for melanocortin-4 receptor-regulated appetite.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

View Samples
accession-icon GSE18590
DNMT1 Maintains Progenitor Function in Self-Renewing Somatic Tissue
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Progenitor cells maintain self-renewing tissues throughout life by sustaining their capacity for proliferation while suppressing cell cycle exit and terminal differentiation. DNA methylation provides a potential epigenetic mechanism for the cellular memory needed to preserve the somatic progenitor state through repeated cell divisions. DNA methyltransferase 1 (DNMT1) maintains DNA methylation patterns after cellular replication. Although dispensable for embryonic stem cell maintenance, a clear role for DNMT1 in maintaining the progenitor state in constantly replenished somatic tissues, such as mammalian epidermis, is uncharacterized. Here we show that DNMT1 is essential for supporting epidermal progenitor cell function. DNMT1 protein was found enriched in undifferentiated cells, where it was required to retain proliferative stamina and suppress differentiation. In tissue, DNMT1 depletion led to exit from the progenitor cell compartment, premature differentiation and eventual tissue loss. These effects correlated with DNA methylation as genome-wide analysis revealed that a significant portion of epidermal differentiation gene promoters were methylated in self-renewing conditions but were subsequently demethylated during differentiation.

Publication Title

DNMT1 maintains progenitor function in self-renewing somatic tissue.

Sample Metadata Fields

Sex, Specimen part

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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