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accession-icon SRP144983
LPS Sensing Mounts an Adaptive MSC Response Enhancing Neutrophil Activation and Wound Healing
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We here addressed the question whether the unique capacity of mesenchymal stromal/stem cells (MSCs) to re-establish tissue homeostasis depends on their potential to sense pathogen associated molecular pattern (PAMP) and, in consequence, mount an adaptive response in the interest of tissue repair. After injection of MSCs which had been primed with the bacterial wall component LPS into murine wounds, an unexpected acceleration of healing occurred, clearly exceeding that of non-primed MSCs. This correlates with a fundamental reprogramming of the transcriptome in LPS treated MSCs as deduced from RNA-seq analysis and its validation. A network of genes mediating the adaptive response through the TLR-4 pathway responsible for neutrophil activation (GCP- 2, ENA-78, IL-1ß IL-8) and MSC protection (SOX6) profoundly contributes to enhanced wound healing. In fact, silencing of either TRL-4, or IRAK3, a downstream effector of TRL-4, or SOX6 suppressed wound healing most likely due to suppression of neutrophil extracellular trap formation and suppression of the enhanced microbicidal release of reactive oxygen species (ROS), key features of neutrophil activation. This previously unreported results uncover SOX6 which protects MSCs at the wound site from enhanced oxidative stress. This unprecedented findings hold substantial promise to refine current MSC-based therapies for difficult-to-treat wounds. Overall design: Transcriptome profiling of MSCs

Publication Title

TLR4-dependent shaping of the wound site by MSCs accelerates wound healing.

Sample Metadata Fields

Treatment, Subject

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accession-icon SRP124942
Identification of immune-activated Hematopoietic Stem Cells
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We utilized our transgenic Fgd5-mCherry mouse to sort and RNAseq for HSCs under acute immune activation (with pIC) to reveal a complex cell cycle gene expression and an upregulated IFN I/II signature Overall design: RNAseq of bone marrow Lineage-Sca1+cKit+CD150+mCherry+ cells (1000) 24hrs after pIC was administered and control (PBS treated)

Publication Title

Identification of immune-activated hematopoietic stem cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE144901
CLL intraclonal fractions exhibit established and recently-acquired patterns of DNA methylation
  • organism-icon Homo sapiens
  • sample-icon 103 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

CLL intraclonal fractions exhibit established and recently acquired patterns of DNA methylation.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE144896
CLL intraclonal fractions exhibit established and recently-acquired patterns of DNA methylation [GE]
  • organism-icon Homo sapiens
  • sample-icon 103 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Intraclonal subpopulations of circulating chronic lymphocytic leukemia (CLL) cells with different proliferative histories and reciprocal surface expression of CXCR4 and CD5 have been observed in the peripheral blood of CLL patients and named proliferative (PF), intermediate (IF) and resting (RF) cellular fractions. Transcriptional differences between paired intraclonal fractions confirmed their proliferative experience and further supported a linear advancement from PF to RF in the peripheral blood. Marked expression differences in intraclonal fractions suggest potential pathological and therapeutic relevance of studying intraclonal CLL fractions as compared to bulk cells.

Publication Title

CLL intraclonal fractions exhibit established and recently acquired patterns of DNA methylation.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE15939
Transcript profiling in LTR mutants
  • organism-icon Arabidopsis thaliana
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

STN7-dependent phosphorylation of an as yet unknown thylakoid protein triggers the signaling events associated with the long-term acclimatory response (LTR). The LTR-associated signaling events regulate the expression of photosynthesis-related genes on the post-transcriptional level (nucleus), as indicated by transcript profiling in LTR mutants.

Publication Title

Arabidopsis STN7 kinase provides a link between short- and long-term photosynthetic acclimation.

Sample Metadata Fields

Specimen part

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accession-icon GSE41010
Differential roles for MBD2 and MBD3 at methylated CpG islands, active promoters and exon sequences
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Differential roles for MBD2 and MBD3 at methylated CpG islands, active promoters and binding to exon sequences.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE41003
Expression data from HeLa cells after MBD2 and MBD3 knock down
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The heterogeneous collection of NuRD complexes can be grouped into the MBD2 or MBD3 containing complexes MBD2-NuRD and MBD3-NuRD. MBD2 is known to bind to methylated CpG sequences in vitro in contrast to MBD3. Although functional differences have been described, a direct comparison of MBD2 and MBD3 in respect to genome-wide binding and function has been lacking. Here we show when depleting cells for MBD2, the MBD2 bound genes increase their activity, whereas MBD2 plus MBD3 bound genes reduce their activity. Most strikingly, MBD3 is enriched at active promoters, whereas MBD2 is bound at methylated promoters and enriched at exon sequences of active genes. This suggests a functional connection between MBD2 binding to chromatin and splicing.

Publication Title

Differential roles for MBD2 and MBD3 at methylated CpG islands, active promoters and binding to exon sequences.

Sample Metadata Fields

Cell line

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accession-icon GSE65459
Knockdown of TSPAN8 gene expression in the SH-SY5Y neuroblastoma cell line
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Bipolar disorder (BD) has an estimated heritability of about 80%. Different pathways and candidate genes may contribute to the pathogenesis of BD, but definite mechanisms are yet unresolved. In a previous study, we identified the single nucleotide polymorphism (SNP) rs4500567, located in the upstream region of Tetraspanin 8 (TSPAN8), to be associated with bipolar disorder (BD).

Publication Title

The regulation of tetraspanin 8 gene expression-A potential new mechanism in the pathogenesis of bipolar disorder.

Sample Metadata Fields

Cell line

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accession-icon GSE38987
Commonly altered genomic regions in acute myeloid leukemia are enriched for somatic mutations involved in chromatin-remodeling and splicing
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Acute myeloid leukemia (AML) is characterized by molecular heterogeneity. As commonly altered genomic regions point to candidate genes involved in leukemogenesis, we used microarray-based comparative genomic hybridization and single nucleotide polymorphism profiling data of 391 AML cases to further narrow down genomic regions of interest. Targeted-resequencing of 1000 genes located in the critical regions was performed in a representative cohort of 50 AML samples comprising all major cytogenetic subgroups. We identified 120 missense/nonsense mutations as well as 60 insertions/deletions affecting 73 different genes (~3.6 tumor-specific aberrations/AML). While most of the newly identified alterations were non-recurrent, we observed a number of mutations affecting genes involved in epigenetic regulation including known candidates like TET2, TET1, DNMT3A and DNMT1, as well as mutations in the histone methyltransferases NSD1, EZH2 and MLL3. Furthermore, we found mutations in the splicing factor SFPQ and in the non-classical regulators of mRNA-processing CTCF and RAD21. These splicing-related mutations affected 10% of AML patients in a mutually exclusive manner. In conclusion, we could identify a significant enrichment of alterations in genes involved in aberrant splicing and epigenetic regulation in genomic regions commonly altered in AML, highlighting their important role in the molecular pathogenesis of AML.

Publication Title

Commonly altered genomic regions in acute myeloid leukemia are enriched for somatic mutations involved in chromatin remodeling and splicing.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE47209
Differential regulation of gene expression by two isoforms of the human transcriptional coactivator MKL1
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We identified two isoforms of human MKL1 that differ in their N-terminal domains. Since MKL1 is a transcriptional coactivator of SRF and regulates many SRF target genes, we wanted to analyze if transcription is differentially regulated by the two isoforms upon stimulation of the Rho-actin-MKL1-SRF pathway.

Publication Title

TGF-β-induced differentiation into myofibroblasts involves specific regulation of two MKL1 isoforms.

Sample Metadata Fields

Cell line

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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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