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accession-icon GSE67242
Analysis of the role of miR-21 in liver regeneration after partial hepatectomy (PHx) in chronic ethanol-treated rats through in vivo inhibition using LNAs
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

In this study, we analyzed the role of miR-21 in liver regeneration after partial hepatectomy (PHx) in chronic ethanol-treated rats. Male Sprague-Dawley rats were fed a liquid diet containing 36% of total calories derived from ethanol for 5 weeks; corresponding pair-fed calorie-matched controls were fed diets in which ethanol calories were replaced by carbohydrate. After 5 weeks, locked nucleic acid (LNA)-modified oligo antisense to miR-21 (AM21, Exiqon, Vedbaek, Denmark) was used to inhibit miRNA in vivo, and rats were subjected to 70% PHx. Liver samples were collected at 24h after the surgery. The excised liver samples at t=0 served as within-animal controls. Rat Gene 2.0 ST (Affymetrix, Santa Clara, CA) arrayswere used to obtain global gene expression data from pooled liver samples (pools of 3 or 4 biological replicates/array, total 8 arrays).

Publication Title

Inhibition of miR-21 rescues liver regeneration after partial hepatectomy in ethanol-fed rats.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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accession-icon SRP112533
Transcriptome analysis of V336Y mutant mitochondrial ribosomal protein in human HEK293 cell line
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Analysis of HEK293 cells lines expressing V336Y mutant mitochondrial ribosomal protein. Overall design: mRNA profiles of wild-type and V336Y mutant HEK293 cell culture samples generated by deep sequencing.

Publication Title

Mutant MRPS5 affects mitoribosomal accuracy and confers stress-related behavioral alterations.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE69801
Analysis of the role of Micu1 in maintaining functional homeostasis in mouse liver
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

In this study, we analyzed global liver gene expression in MICU1 knock-down (KD) mice. To generate liver-specific MICU1 KD mice, MICU1loxp/loxp male mice were treated with an AAV8-Cre under the control of a hepatocyte specific promoter (TBG). AAV8-TBG-Null treated littermates were used as controls. Liver samples were collected 3-5 weeks after injection. Knockdown was verified by protein and mRNA (94%, 98%, respectively). Mouse Gene 2.0 ST (Affymetrix, Santa Clara, CA) arrays were used to obtain global gene expression data.

Publication Title

MICU1 regulation of mitochondrial Ca(2+) uptake dictates survival and tissue regeneration.

Sample Metadata Fields

Treatment

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accession-icon GSE487
PGA Rat Liver Methylprednisolone
  • organism-icon Rattus norvegicus
  • sample-icon 91 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

Summary: The liver is the major site of gluconeogenesis, fat processing and distribution, as well as drug and xenobiotic metabolism. Altered gene expression in the liver is centrally invovled in both the immuosuppressive and the energetic actions of corticosteroids.

Publication Title

Modeling of corticosteroid pharmacogenomics in rat liver using gene microarrays.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE1721
Rat Kidney Methylprednisolone
  • organism-icon Rattus norvegicus
  • sample-icon 63 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

Summary: To identify distinct temporal patterns of mRNA expression in the kidney of rats following a bolus dose of the corticosteroid methylprednisolone.

Publication Title

Corticosteroid-regulated genes in rat kidney: mining time series array data.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE25612
Circadian regulation in rat Lung
  • organism-icon Rattus norvegicus
  • sample-icon 54 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Circadian rhythms are oscillations with a periodicity of 24 hours that are controlled by an endogenous clock and are observed in virtually all aspects of mammalian function from expression of genes to complex physiological processes. The master clock is present in the suprachiasmatic nucleus (SCN) in the anterior part of the hypothalamus and controls peripheral clocks present in other parts of the body . Although much is known about the mechanism of the central clock in the SCN, the regulation of clocks present in peripheral tissues is still unclear. This study is designed to examine fluctuations in gene expression in lungs within the 24 hour circadian cycle in normal animals. The objectives of this study is to identify and analyze circadian oscillation in gene expression in lungs, and to identify the role of circadian regulation in coordinating the functioning of this dynamic organ.

Publication Title

Light-dark oscillations in the lung transcriptome: implications for lung homeostasis, repair, metabolism, disease, and drug action.

Sample Metadata Fields

Specimen part

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accession-icon GSE490
Pharmacogenomic effect of corticosteroid in skeletal muscle
  • organism-icon Rattus norvegicus
  • sample-icon 51 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

The aim of this project is to identify distinct temporal patterns of RNA expression in the skeletal muscle of rats following a bolus dose of the corticosteroid methylprednisolone. 51 RG_U34A chips were used over 17 time points.

Publication Title

Temporal profiling of the transcriptional basis for the development of corticosteroid-induced insulin resistance in rat muscle.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20635
Circadian regulation in rat abdominal adipose tissue
  • organism-icon Rattus norvegicus
  • sample-icon 52 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Circadian rhythms are oscillations with a periodicity of 24 hours that are controlled by an endogenous clock and are observed in virtually all aspects of mammalian function from expression of genes to complex physiological processes. The master clock is present in the suprachiasmatic nucleus (SCN) in the anterior part of the hypothalamus and controls peripheral clocks present in other parts of the body. Although much is known about the mechanism of the central clock in the SCN, the regulation of clocks present in peripheral tissues is still unclear. This study is designed to examine fluctuations in gene expression in abdominal white adipose tissue within the 24 hour circadian cycle in normal animals. The objectives of this study is to identify and analyze circadian oscillation in gene expression in white adipose tissue, and to identify the role of circadian regulation in coordinating the functioning of this dynamic tissue.

Publication Title

Circadian variations in gene expression in rat abdominal adipose tissue and relationship to physiology.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE13271
Diabetes biomarker disease progression study in rat liver, gastrocnemius muscle, and adipose tissue
  • organism-icon Rattus norvegicus
  • sample-icon 301 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Gene expression analysis of hepatic roles in cause and development of diabetes in Goto-Kakizaki rats.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE13268
Diabetes biomarker disease progression study in rat adipose tissue
  • organism-icon Rattus norvegicus
  • sample-icon 100 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The goals and objectives: To study Type 2 diabetes progression and the development of insulin resistance in two animal models with and without a high fat diet superimposed on these models. Background: Diabetes is a systemic metabolic imbalance involving multiple tissues/organs, and an early hallmark feature of this disease state is insulin resistance. Multifactorial interactions of genetics, prenatal environmental factors (fetal programming) and postnatal environmental factors (nutrition and activity) likely contribute to the diabetic phenotype.Animal models can serve as a valuable tool for studying diabetes disease progression and for identifying useful biomarkers of type 2 diabetes. Several inbred rodent models are available for diabetes related studies. The GK rat is an obvious choice among available inbred models as the genetic basis for this inheritable form of diabetes is polygenic (5), unlike most other inbred rodent models that exhibit single gene defects. Many of the characteristics of the GK rat mirror human diabetes (hyperglycemia, glucose intolerance, insulin resistance), although hyperlipidemia does not appear to be prominent in the GK rat. Due to its polygenic mode of inheritance and 100% penetrance, the GK rat may be a useful model for human diabetes. Induced animal models can also be useful in diabetes studies. One such model is metabolic syndrome resulting from experimentally induced fetal programming (produced by maternal malnutrition or by exposure to corticosteroids in the third trimester). Both in humans and animals, accumulating evidence suggests that alterations in the human fetal environment can result in permanent physiologic changes that manifest as increased incidence of adult onset pathology. Numerous epidemiological studies have forged a strong link between low birth weight and the development of metabolic syndrome in adulthood. From such observations has arisen the concept of fetal programming whereby exposure to some factor(s) during crucial stages in development can permanently alter or reset physiologic/metabolic functions. In the rat, exposure to corticosteroids during a window in third trimester gestation (CS programming) results in fetal growth retardation and insulin resistance in adult offspring. Genetic factors play a primarily role in the etiology of diabetes in the GK rat, whereas fetal environmental factors are causative in CS programming. (It should be noted that although altered fetal environmental effects, most likely stemming from maternal hyperglycemia, have been implicated to play some role in the decreased pancreatic B cell mass in GK rats, these effects occur earlier in gestation and therefore differ from programming by CS in late gestation.) A comparison of the development of insulin resistance in the GK rat with development in the CS programmed rat will provide insight into genetic and fetal environmental factors in disease development. Superimposing dietary alterations (i.e., high fat feeding) (11) on both animal models may aid in the dissection of multiple interacting factors (genetic, fetal environmental factors, postnatal environmental factors) on the development and progression of insulin resistance and type 2 diabetes. Such studies may also aid in the identification of useful biomarkers for insulin resistance and type 2 diabetes in humans.

Publication Title

Gene expression analysis of hepatic roles in cause and development of diabetes in Goto-Kakizaki rats.

Sample Metadata Fields

No sample metadata fields

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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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