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accession-icon GSE25485
Gene expression data in Bone Marrow Derived Dendritic Cells (BMDC) following nanoemulsion adjuvant exposure
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Antigen uptake, processing and presentation by dendritic cells are regulated by complex intra- and inter-cellular signalling events. Typical vaccine adjuvants lead to the transcription of pro-inflammatory cytokines and chemokines which relate to immune induction.

Publication Title

Nanoemulsion mucosal adjuvant uniquely activates cytokine production by nasal ciliated epithelium and induces dendritic cell trafficking.

Sample Metadata Fields

Sex, Age, Specimen part, Time

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accession-icon SRP047487
mRNA- and RISC-sequencing of mouse hearts overexpressing miR-378a
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon

Description

Rationale: MicroRNAs play key roles in hypertrophic stress responses. miR-378(-3p) is a highly abundant, cardiomyocyte-enriched microRNA whose downregulation in pressure-overload has been suggested as detrimental to the heart. Previous studies have utilized systemic anti-miR or microRNA-encoding virus administration, and thus questions regarding the cardiomyocyte-autonomous roles of miR-378 remain. Objective: To examine whether persistent overexpression of miR-378 in cardiomyocytes alters the phenotype of the unstressed heart, whether its overexpression is beneficial or deleterious in the setting of pressure-overload, and to comprehensively identify its cardiomyocyte-specific effects on mRNA regulation. Methods and Results: Cardiac function was compared in young (10-12 week-old) mice overexpressing miR-378 in the heart under the control of the Myh6 promoter (alphaMHC-miR-378 mice), in older (40 week-old) mice and their age-matched wild-type controls. Older alphaMHC-miR-378 mice exhibited decreased fractional shortening and modest chamber dilation with an increase in cardiomyocyte length. When subjected to pressure-overload, cardiomyocyte length was increased in young alphaMHC-miR-378 mice, but fractional shortening declined precipitously over two weeks. Transcriptome profiling of wild-type and alphaMHC-miR-378 hearts in unstressed and pressure-overload conditions revealed dysregulation of several upstream metabolic and mitochondrial genes in alphaMHC-miR-378 hearts, compromising the reprogramming that occurs during early adaptation to pressure overload. Ago2 immunoprecipitation with mRNA sequencing revealed novel miR-378 cardiac mRNA targets including Akt1 and Epac2 and demonstrated the contextual nature of previously described miR-378 targeting events. Conclusions: Long-term upregulation of miR-378 levels in the heart is not innocuous and exacerbates contractile dysfunction in pressure-overload hypertrophy through numerous signaling mechanisms. Overall design: Cardiac polyadenylated RNA (mRNA) or RISC-seq (total RNA-seq of Ago2 immunoprecipitate) profiles were generated from nontransgenic and transgenic mouse hearts of FVB/N background, on Illumina HiSeq 2000 instruments. Male mice 8-12 weeks of age were used in these studies, and subjected to sham surgery or 2 weeks of pressure-overload via transverse aortic constriction (TAC). 3 nontransgenic sham, 3 transgenic sham, 7 nontransgenic TAC, 7 transgenic TAC, each with mRNA-seq and RISC-seq data.

Publication Title

Cardiac Disease Status Dictates Functional mRNA Targeting Profiles of Individual MicroRNAs.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP052702
mRNA- and RISC-sequencing of mouse hearts overexpressing miR-133a
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon

Description

miR-133a-3p is a highly abundant cardiomyocyte-enriched microRNA whose expression is persistently decreased in response to pressure overload (or transverse aortic constriction, TAC) in mice. Overexpression of miR-133a in cardiomyocytes of mouse hearts in vivo (under the control of the Myh6 promoter) decreases pressure overload-induced apoptosis and fibrosis. In previous studies using microarray platforms, we detected numerous mRNAs whose transcript levels were altered by either or both of miR-133a overexpression and pressure overload. The data set presented here builds upon our previous study in these mice by examining mRNA-RISC associations (using Ago2-immunoprecipitated RNA) and global mRNA abundances via RNA-sequencing procedures, and tests the hypothesis that mRNAs targeted by overexpressed miR-133a are dissimilar between sham and TAC contexts. Overall design: Cardiac polyadenylated RNA (mRNA) profiles were generated from nontransgenic and transgenic mouse hearts of FVB/N background, on Illumina HiSeq 2000 instruments. Male mice 8-12 weeks of age were used in these studies, and subjected to sham surgery or 1 week of pressure-overload via transverse aortic constriction (TAC). 3 nontransgenic sham, 7 transgenic sham, 5 nontransgenic TAC, 4 transgenic TAC, each with mRNA-seq and RISC-seq (mRNA-seq of Ago2 immunoprecipitate) data.

Publication Title

Cardiac Disease Status Dictates Functional mRNA Targeting Profiles of Individual MicroRNAs.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP043194
Polyadenylated RNA Sequencing of C57BL/6J Embryonic, Adult and Pressure-Overloaded Hearts
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

A few reports have implicated specific lncRNAs in cardiac development or failure, but precise details of lncRNAs expressed in hearts and how their expression may be altered during embryonic heart development or by adult heart disease is unknown. By comparing lncRNA profiles of normal embryonic (~E14), normal adult, and hypertrophied adult hearts we defined a distinct fetal lncRNA abundance signature that includes 157 lncRNAs differentially expressed compared to adults (fold-change = 50%, FDR=0.02), and which was only poorly recapitulated in hypertrophied hearts (17 differentially expressed lncRNAs; 13 of these observed in embryonic hearts). Analysis of protein-coding mRNAs from the same samples identified 22 concordantly and 11 reciprocally regulated mRNAs within 10 kb of dynamically expressed lncRNAs, reciprocal relationships of lncRNA and mRNA levels was validated for the Mccc1 and Relb genes using in vitro lncRNA knockdown in C2C12 cells. Network analysis suggested a central role for lncRNAs in modulating NFkappaB- and CREB1-regulated genes during embryonic heart growth and identified multiple mRNAs within these pathways that are also regulated, but independently of lncRNAs. Overall design: Cardiac polyadenylated RNA (mRNA and lncRNA) profiles were generated from C57BL/6J mouse hearts were generated on Illumina HiSeq 2000 instruments. 7 independent E13.5 hearts, 12 adult hearts (6 at 6 weeks of age, 6 at 16 weeks of age), 4 sham-operated hearts at 12 weeks of age, and 4 hearts after 4 weeks of pressure overload (TAC) at 12 weeks of age.

Publication Title

Epigenetic coordination of embryonic heart transcription by dynamically regulated long noncoding RNAs.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP043191
Next Generation Sequencing of Wild-Type FVB/NJ Mouse Primary Cardiomyocyte and Cardiac Nonmyocyte Polyadenylated RNA and small RNA
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Cells from three adult, wild-type, FVB hearts were separated into cardiomyocyte and nonmyocyte fractions using Langendorff perfusion, collagenase digestion and gravity filtration. Total RNA was prepared immediately from myocytes, while nonmyocytes were passaged twice to yield a culture from which total RNA was prepared. Overall design: 6 cardiac polyadenylated RNA (mRNA and lncRNA) and small RNA (microRNA) profiles of isolated cardiomyocytes (CM) and nonmyocytes (fibro) from 12-wk FVB/NJ mouse hearts were generated on Illumina HiSeq 2000 instruments.

Publication Title

Epigenetic coordination of embryonic heart transcription by dynamically regulated long noncoding RNAs.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP041258
Next Generation Sequencing of Wild-Type FVB/NJ Mouse Cardiac Polyadenylated RNA After 1 Week Pressure Overload
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Next-generation sequencing (NGS) provides for quantitation of RNA abundances and comparison of RNA abundances within tissues and cells in a manner not possible with previous microarray technologies. 5 female mice were subjected to a sham operation, and 5 female mice were subjected to transverse aortic constriction (TAC). After 1 week, hearts were harvested and polyadenylated RNAs were profiled. Analyzed data have been published in Hu et al., Proc Natl Acad Sci USA. 2012;109(48):19864-9, PMID: 23150554 Overall design: 10 cardiac polyA+-RNA profiles of 9 week-old FVB/NJ wild type (WT) mice (5 female sham, 5 female TAC) were generated on Illumina HiSeq 2000 instruments.

Publication Title

Epigenetic coordination of embryonic heart transcription by dynamically regulated long noncoding RNAs.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP039962
Next Generation Sequencing of Wild-Type FVB/NJ Mouse Cardiac Small RNA
  • organism-icon Mus musculus
  • sample-icon 39 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Next-generation sequencing (NGS) provides for quantitation of RNA abundances and comparison of RNA abundances within tissues and cells in a manner not possible with previous microarray technologies. We have made widespread use of Illumina sequencing technologies for RNA quantitation in several publications involving mouse hearts, dating from 2010, and wish to share both high-quality raw sequencing data and data processed to quantitate mRNA abundances from wild-type mice, male and female, at a variety of ages. These data will provide a resource for investigators using microarrays to understand the concentration of transcripts of interest relative to other cardiac RNAs, and will permit deeper interpretation of previous microarray studies. Overall design: 39 cardiac small RNA (microRNA) profiles of 4- to 16 week-old FVB/NJ wild type (WT) mice were generated on Illumina HiSeq 2000 instruments.

Publication Title

Great Expectations: MicroRNA-30d and Cardiac Resynchronization Therapy.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP065536
Adult-induced cardiac-specific knockout of Parkin provokes minimal transcriptional effect
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Adult mice bearing homozygous floxed Parkin alleles (PMIDs 15249681, 21376232; T M Dawson), with or without the Myh6-driven MERCreMER transgene, were administered tamoxifen at 6-10 wks of age. Tissues were obtained from euthanized mice 9-10 weeks after tamoxifen induction. Overall design: 6 floxed, non-Cre (noninduced) mouse hearts; 6 floxed, MERCreMer, adult-induced, Parkin knockout mouse hearts

Publication Title

Central Parkin: The evolving role of Parkin in the heart.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon SRP065537
Mitochondrial contagion induced by Parkin deficiency in Drosophila hearts and its containment by suppressing mitofusin; germline Parkin knockout mouse hearts.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Dysfunctional Parkin-mediated mitophagic culling of senescent or damaged mitochondria is a major pathological process underlying Parkinson disease and a potential genetic mechanism of cardiomyopathy. Despite epidemiological associations between Parkinson disease and heart failure, the role of Parkin and mitophagic quality control in maintaining normal cardiac homeostasis is poorly understood.We used germline mutants and cardiac-specific RNA interference to interrogate Parkin regulation of cardiomyocyte mitochondria and examine functional crosstalk between mitophagy and mitochondrial dynamics in Drosophila heart tubes. Overall design: 5 wild-type mouse hearts; 4 germline Parkin knockout mouse hearts Please note that the mouse cardiac examples were an adjunct to the Drosophila studies that comprised most of the associated publication. However, mRNA-sequencing was only performed on the mouse samples, not the Drosophila heart tubes.

Publication Title

Central Parkin: The evolving role of Parkin in the heart.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP039959
Next Generation Sequencing of Wild-Type C57BL/6J Mouse Cardiac Small RNA
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Next-generation sequencing (NGS) provides for quantitation of RNA abundances and comparison of RNA abundances within tissues and cells in a manner not possible with previous microarray technologies. We have made widespread use of Illumina sequencing technologies for RNA quantitation in several publications involving mouse hearts, dating from 2010, and wish to share both high-quality raw sequencing data and data processed to quantitate mRNA abundances from wild-type mice, male and female, at a variety of ages. These data will provide a resource for investigators using microarrays to understand the concentration of transcripts of interest relative to other cardiac RNAs, and will permit deeper interpretation of previous microarray studies. Overall design: 6 cardiac small RNA (microRNA) profiles of 18 week-old C57BL/6J wild type (WT) mice were generated on Illumina HiSeq 2000 instruments.

Publication Title

Menage a Trois: intimate relationship among a microRNA, long noncoding RNA, and mRNA.

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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