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accession-icon GSE65173
NF-B activation impairs somatic cell reprogramming in ageing
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Gene 2.0 ST Array (hugene20st), Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

NF-κB activation impairs somatic cell reprogramming in ageing.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment

View Samples
accession-icon GSE85269
Expression data of intact and ventilated wildtype and Zmpste24-deficient mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

To study how changes in the nuclear mechanical properties may modify the development of Ventilator-induced lung injury, mice of both genotypes were studied at baseline or after 2.5 hours of mechanical ventilation (PIP 15cmH2O, ZEEP, 100 breaths/min, inspiratory:expiratory ratio 1:1, inpired oxygen fraction 0.21).After that, mice were sacrificed, the lungs estracted and gene expression measured in order to identify the differential gene expression depending on the different nuclear stifness.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE117188
Effect of methione restriction in the liver of WT and Lmna G609G KI mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Dietary intervention constitutes a feasible approach for modulating metabolism and improving healthspan and lifespan. Methionine restriction (MR) delays the appearance of age-related diseases and increases longevity in normal mice. However, the effect of MR on premature aging remains to be elucidated. Here, we describe that MR extends lifespan in two different mouse models of Hutchinson-Gilford progeria syndrome (HGPS) by reversing the transcriptome alterations in inflammation and DNA-damage response genes present in this condition. Further, MR improves the lipid profile and alters the levels of bile acids, both in wild-type and in progeroid mice. Notably, treatment with the bile acid cholic acid improves healthspan and lifespan in vivo. These results suggest the existence of a metabolic pathway involved in the longevity extension achieved by MR and support the possibility of dietary interventions for treating progeria.

Publication Title

Methionine Restriction Extends Lifespan in Progeroid Mice and Alters Lipid and Bile Acid Metabolism.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE84900
Differential gene expression on islet transplantation with or without the presence of autologous fibroblasts
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Pancreatic islet transplantation was performed in the subcutaneous space of diabetic nude mice. In order to promote long survival and function of transplanted islets a plasma-based scaffold was developed in combination with fibroblasts as graft-supporting accesory cells. Gene expression analysis was carried out to evaluate expression differences due to the presence of fibroblast which could explain the long-term glycemic control observed under these circumstances.

Publication Title

Fibroblasts accelerate islet revascularization and improve long-term graft survival in a mouse model of subcutaneous islet transplantation.

Sample Metadata Fields

Disease, Time

View Samples
accession-icon GSE36056
Transcriptional profiling of intestinal samples from Atg4b knock-out mice during chemical-induced colitis
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The identification of inflammatory bowel disease (IBD) susceptibility genes by genome-wide association has linked this pathology to autophagy, a lysosomal degradation pathway that is crucial for cell and tissue homeostasis. Here, we describe autophagin-1 (ATG4B) as an essential protein in the control of inflammatory response during experimental colitis. In this pathological condition, ATG4B protein levels increase paralleling the induction of autophagy. Moreover, ATG4B expression is significantly reduced in affected areas of the colon from IBD patients. Consistently, atg4b-/- mice present Paneth cell abnormalities, as well as an increased susceptibility to DSS-induced colitis. Atg4b-deficient mice exhibit significant alterations in proinflammatory cytokines and mediators of the immune response to bacterial infections, which are reminiscent of those found in patients with Crohns disease or ulcerative colitis. Additionally, antibiotic treatments and bone marrow transplantation from wild-type mice reduced colitis in atg4b-/- mice. Taken together, these results provide additional evidence on the importance of autophagy in intestinal pathologies and describe ATG4B as a novel protective protein in inflammatory colitis. Finally, we propose that Atg4b-null mice are a suitable model for in vivo studies aimed at testing new therapeutic strategies for intestinal diseases associated with autophagy deficiency

Publication Title

ATG4B/autophagin-1 regulates intestinal homeostasis and protects mice from experimental colitis.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

View Samples
accession-icon GSE65783
Expression data from intact and ventilation-preconditioned murine lungs
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

To study the effects of previous exposure to mechanical ventilation may modify the development of Ventilator-induced lung injury, preconditioning was induced by low-pressure ventilation for 90 minutes. After 1 week, intact (sham) and preconditioned mice were sacrificed, the lungs extracted and gene expression measured in order to identify differences responsible for the observed tolerance to ventilator-induced lung injury observed in preconditioned animals.

Publication Title

Exposure to mechanical ventilation promotes tolerance to ventilator-induced lung injury by Ccl3 downregulation.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE65172
NF-B activation impairs somatic cell reprogramming in ageing [MSCs]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Transcriptional profiling of human control and Nstor-Guillermo Progeria Syndrome (NGPS) mesenchymal stem cells (MSCs).

Publication Title

NF-κB activation impairs somatic cell reprogramming in ageing.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment

View Samples
accession-icon GSE71922
Loss of the proteostasis modulator AIRAPL causes myeloid transformation by deregulating IGF-1 signaling
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Transcriptional profiling of human acute myeloid leukemia cells lines HEL and SET2 transduced with an IGF1R shRNA and miR-125a sponge.

Publication Title

Loss of the proteostasis factor AIRAPL causes myeloid transformation by deregulating IGF-1 signaling.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE32609
Transcriptional profiling of liver samples from Lmna Gly609Gly knock-in mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have allowed the recent development of the first therapeutic approaches for this disease. However, none of these earlier works have addressed the aberrant and pathogenic LMNA splicing observed in HGPS patients because of the lack of an appropriate mouse model. We report herein a genetically modified mouse strain that carries the HGPS mutation. These mice accumulate progerin, present histological and transcriptional alterations characteristic of progeroid models, and phenocopy the main clinical manifestations of human HGPS, including shortened life span and bone and cardiovascular aberrations. By using this animal model, we have developed an antisense morpholinobased therapy that prevents the pathogenic Lmna splicing, dramatically reducing the accumulation of progerin and its associated nuclear defects. Treatment of mutant mice with these morpholinos led to a marked amelioration of their progeroid phenotype and substantially extended their life span, supporting the effectiveness of antisense oligonucleotidebased therapies for treating human diseases of accelerated aging.

Publication Title

Splicing-directed therapy in a new mouse model of human accelerated aging.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE40529
Expression data from untreated and DSS-treated Adamts12 WT and KO mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Adamts12-deficient mice undergo more severe colitis than WT mice after induction with DSS.

Publication Title

ADAMTS-12 metalloprotease is necessary for normal inflammatory response.

Sample Metadata Fields

Specimen part, Treatment

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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