Macrophages have distinct characteristics depending on their microenvironment. We performed proteomic analysis between M1 and M2 macrophages and found that cellular metabolism is the key regulator of macrophage function.
Proteomic Analysis Reveals Distinct Metabolic Differences Between Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) and Macrophage Colony Stimulating Factor (M-CSF) Grown Macrophages Derived from Murine Bone Marrow Cells.
Specimen part
View SamplesPurpose: 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.
Great Expectations: MicroRNA-30d and Cardiac Resynchronization Therapy.
No sample metadata fields
View SamplesAdult 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
Central Parkin: The evolving role of Parkin in the heart.
Specimen part, Subject, Time
View SamplesDysfunctional 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.
Central Parkin: The evolving role of Parkin in the heart.
Specimen part, Subject
View SamplesPurpose: 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.
Menage a Trois: intimate relationship among a microRNA, long noncoding RNA, and mRNA.
No sample metadata fields
View SamplesPurpose: 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 (see our FVB/NJ data submission). 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: 4 cardiac polyA+-RNA profiles of 12 week-old C57BL/6J wild type (WT) mice were generated on Illumina HiSeq 2000 instruments.
Menage a Trois: intimate relationship among a microRNA, long noncoding RNA, and mRNA.
No sample metadata fields
View SamplesRationale: 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.
Cardiac Disease Status Dictates Functional mRNA Targeting Profiles of Individual MicroRNAs.
No sample metadata fields
View SamplesmiR-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.
Cardiac Disease Status Dictates Functional mRNA Targeting Profiles of Individual MicroRNAs.
No sample metadata fields
View SamplesTFIID is a central player in activated transcription initiation. Recent evidence suggests that the role and composition of TFIID is more diverse than previously understood. To investigate the effects of changing the composition of TFIID in a simple system we depleted TAF1 from Drosophila cells and determined the consequences on metal induced transcription at an inducible gene, Metallothionein B (MtnB). We observe a marked increase in the levels of both the mature message and pre-mRNA in TAF1 depleted cells. Under conditions of continued metal exposure, we show that TAF1 depletion increases the magnitude of the initial transcription burst, but has no effect on the timing of that burst. We also show that TAF1 depletion causes delay in the shut-off of transcription upon removal of the stimulus. Thus TAFs are involved in both establishing an upper limit of transcription during induction and efficiently turning the gene off once the inducer is removed. Using genomewide nascent-seq we identify hundreds of genes that are controlled in a similar manner indicating that the findings at this inducible gene are likely generalizable to a large set of promoters. There is a long-standing appreciation for the importance of the spatial and temporal control of transcription. Here we uncover an important third dimension of control, the magnitude of the response. Our results show that the magnitude of the transcriptional response to the same signaling event, even at the same promoter, can vary greatly depending on the composition of the TFIID complex in the cell. Overall design: Nascent RNA was sequenced from replicate samples of Drosophila S2 cells treated with double-stranded RNA directed against E. coli LacI (Control) or against Drosophlia TAF1 (experimental). Reads per kilo-base per million (RPKM) was determined for each gene and the control and experimental samples were compared to determine the genes that were affected by the depletion of TAF1.
Holo-TFIID controls the magnitude of a transcription burst and fine-tuning of transcription.
Specimen part, Subject
View SamplesThe leaf of Eriobotrya japonica (Ej) has been used for a long time as an oriental medicine to treat pulmonary inflammatory diseases.
Protective changes of inflammation-related gene expression by the leaves of Eriobotrya japonica in the LPS-stimulated human gingival fibroblast: microarray analysis.
Specimen part, Treatment
View Samples