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Links from GEO DataSets

Items: 20

1.

Overexpression of A kinase interacting protein 1 attenuates myocardial ischemia / reperfusion injury, but does not influence heart failure development

(Submitter supplied) Aims A kinase interacting protein 1 (AKIP1) stimulates physiological growth in cultured cardiomyocytes and attenuates ischemia / reperfusion (I/R) injury in ex vivo perfused hearts. We aimed to determine whether AKIP1 modulates the cardiac response to acute and chronic cardiac stress in vivo. Methods and results Transgenic mice with cardiac-specific overexpression of AKIP1 (AKIP1-TG) were created. AKIP1-TG mice and their wild type (WT) littermates displayed similar cardiac structure and function. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
16 Samples
Download data: TXT
Series
Accession:
GSE83472
ID:
200083472
2.

Role of Sirt1 in cardiomyocytes in the development of caloric restriction-induced cardioprotection

(Submitter supplied) Comparison of transcriptional profiling in murine hearts obtained from the control mice fed ad libitium (AL) and treated with caloric restriction (CR). Comparison of transcriptional profiling in murine hearts obtained from cardiomyocye-specific Sirt1 knockout mice fed ad libitium and treated with caloric restriction.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL5642
2 Samples
Download data: TXT
Series
Accession:
GSE75558
ID:
200075558
3.

Myocardial G protein-coupled receptor kinase 5 contributes to impaired cardiac function and immune cell recruitment in ischemic heart failure

(Submitter supplied) Myocardial ischemia (MI) is the most common cause of heart failure (HF) in the United States. G protein‑coupled receptor (GPCR) kinase 5 (GRK5) has been found to be upregulated in failing human myocardium. While the canonical role of GRKs is to desensitize receptors via phosphorylation, GRK5 can also translocate to the nucleus of cardiomyocytes where it exerts GPCR‑independent effects that promote maladaptive cardiac hypertrophy. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
10 Samples
Download data: TXT
Series
Accession:
GSE132701
ID:
200132701
4.

miRNA expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

(Submitter supplied) To investigate the role of CITED4 in a murine model of cardiac pressure overload
Organism:
Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL17021
10 Samples
Download data: TXT
Series
Accession:
GSE150293
ID:
200150293
5.

The Role of Endothelial Autocrine NRG1/ERBB4 Signaling in Cardiac Remodeling

(Submitter supplied) Neuregulin-1 (NRG1) is a paracrine growth factor, secreted by cardiac endothelial cells (Ecs) in conditions of cardiac overload/injury. The current concept is that the cardiac effects of NRG1 are mediated by activation of ERBB4/ERBB2 receptors on cardiomyocytes. However, recent studies have shown that paracrine effects of NRG1 on fibroblasts and macrophages are equally important. Here, we hypothesize that NRG1 autocrine signaling plays a role in cardiac remodeling. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
24 Samples
Download data: TSV
Series
Accession:
GSE150619
ID:
200150619
6.

FTO-Dependent m6A Regulates Cardiac Function During Remodeling and Repair

(Submitter supplied) Background: Despite its functional importance in various fundamental bioprocesses, the studies of N6-methyladenosine (m6A) in the heart are lacking. Methods: We performed methylated (m6A) RNA immunoprecipitation sequencing (MeRIP-seq) to map transcriptome-wide m6A in healthy and failing hearts. Results: Improving expression of FTO in failing mouse hearts attenuated the ischemia-induced increase in m6A and decrease in cardiac contractile function. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE112789
ID:
200112789
7.

Effect of cardiac-specific FASTKD1 overexpression on gene expression in the heart

(Submitter supplied) We generated transgenic mice with cardiac myocyte-specific overexpression of the mitochondrial RNA regulating protein FASTKD1 We then harvested hearts from 3-month-old non-transgenic and transgenic mice (4 mice in each group) and conducted gene expression profiling using RNA seq
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE213045
ID:
200213045
8.

Loss of Lin28a Attenuates Cardiac Hypertrophy Induced by Pressure Overload

(Submitter supplied) Pathological cardiac hypertrophy is a major risk factor for the development of heart failure and sudden cardiac death, yet the molecular mechanism of cardiac hypertrophy is not fully understood. Recently, we found that the expression of Lin28a, a RNA-binding protein, was significantly upregulated during the early stages of cardiac hypertrophy. Interestingly, cardiac specific conditional deletion of Lin28a blunted pressure overload-induced cardiac hypertrophic responses. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: CSV
Series
Accession:
GSE106897
ID:
200106897
9.

Microarray analysis of heart gene expression in wild type and JMJD2A heart specific transgenic mice after sham and thoracic aortic constriction surgery

(Submitter supplied) Cardiac hypertrophy and failure are accompanied by a reprogramming of gene expression that involves transcription factors and chromatin remodeling enzymes. Little is known about the role of histone methylation and demethylation in this process. To understand the role of JMJD2A, a trimethyl demethylase for histone 3 lysine 9 and 36, in cardiac hypertrophy, we generated heart specific JMJD2A deletion (JMJD2A hKO) and overexpression (JMJD2A-Tg) mouse lines. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
6 Samples
Download data: TXT
Series
Accession:
GSE27689
ID:
200027689
10.

RNA sequencing of adult cardiomyocyte cyclin C deletion

(Submitter supplied) The goal of this study was to identify differentially expressed genes in hearts with cardiomyoycte deletion of cyclin c compared to cyclin c floxed controls.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: XLSX
Series
Accession:
GSE144947
ID:
200144947
11.

Analysis of mRNA expression in CHAPIR overexpressed heart

(Submitter supplied) To elucidate the molecular mechanism by which cardiac-hypertrophy-associated piRNA (CHAPIR) regulates gene expression, RNA-seq was performed on control or CHAPIR-overexpressing mice heart. Based on RNA-seq data, 720 differentially expressed genes were shown in CHAPIR-overexpressing heart relative to NC control, including 519 upregulated and 201 downregulated genes.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
2 Samples
Download data: XLSX
Series
Accession:
GSE154781
ID:
200154781
12.

Analysis of m6A methylome in CHAPIR overexpressed heart [MeRIP]

(Submitter supplied) To elucidate the molecular mechanism by which cardiac-hypertrophy-associated piRNA (CHAPIR) regulates m6A modification, we performed m6A methylated RNA immunoprecipitation sequencing (MeRIP-seq) in control or CHAPIR-overexpressing mice heart. The sequential analysis of m6A peaks showed that RGACH motif was highly enriched within m6A sites in heart and that is aligning with the classical consensus sequence of mammals ‘RGACH’, where ‘R’ indicates purine (A/G) and ‘H’ indicates non-guanine base (A/C/U). more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL21103
4 Samples
Download data: XLSX
Series
Accession:
GSE154699
ID:
200154699
13.

Differentially Expressed piRNAs in TAC-induced mouse cardiac hypertrophy

(Submitter supplied) To systematically investigate the potential role of piRNA(s) and for the identification of specific piRNA(s) dysregulated in cardiac hypertrophy, we examined the global expression profile of piRNAs in left ventricle samples obtained 4 weeks after TAC surgery in adult mice.
Organism:
Mus musculus
Type:
Non-coding RNA profiling by array
Platform:
GPL22552
2 Samples
Download data: TXT
Series
Accession:
GSE153445
ID:
200153445
14.

ERBB2 drives YAP activation and EMT-like processes during cardiac regeneration

(Submitter supplied) RNA-seq comparing WT and caERBB2 over expresising hearts with/out injury
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
16 Samples
Download data: XLSX
Series
Accession:
GSE144391
ID:
200144391
15.

RNA-Seq Analyses of TGAC8 and WT mouse Left Ventricles

(Submitter supplied) 8 LV samples from WT and TGAC8 mouse hearts were analyzed. Mice were 3 m.o. Human ADCY8 gene was overexpressed in mouse heart under cardiac-specific MYH7 promoter
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
16 Samples
Download data: XLSX
Series
Accession:
GSE205234
ID:
200205234
16.

Cardiac-specific YAP activation improve cardiac function and survival in an experimental murine MI model

(Submitter supplied) In this study, we used a cardiac-specific, inducible expression system to activate YAP in adult mouse heart. Activation of YAP in adult heart promoted cardiomyocyte proliferation and did not deleteriously affect heart function. Furthermore, YAP activation after myocardial infarction (MI) preserved heart function and reduced infarct size. Using adeno-associated virus subtype 9 (AAV9) as a delivery vector, we expressed human YAP in the murine myocardium immediately after MI. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
9 Samples
Download data: CEL
Series
Accession:
GSE54612
ID:
200054612
17.

Exercise Reverses Dysregulated Gene Expression in a Desmoplakin Haplo-insufficient Mouse Model of Arrhythmogenic Cardiomyopathy

(Submitter supplied) Mutations in desmosome genes cause arrhyythmogenic cardiomyopathy (ACM). Using desmoplakin haploinsufficient mouse model of ACM, we evaluated the effects of treadmill exercise on cardiac myocyte transcritional profile. Strand specific, ribosome depleted paired end RNA sequencing of cardiac myocytes from wild type and Myh6-Cre:DspW/F were generate using Illumina HiSeq 4000.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
30 Samples
Download data: TXT
Series
Accession:
GSE129962
ID:
200129962
18.

CaM Kinase II mediates maladaptive post-infarct remodeling but not acute myocardial ischemia/reperfusion injury

(Submitter supplied) Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL18802
18 Samples
Download data: CEL
Series
Accession:
GSE58486
ID:
200058486
19.

Transcriptomes of the hybrid mouse diversity panel subjected to Isoproterenol challenge

(Submitter supplied) Transcriptomes performed on left ventricular heart samples from mice of the hybrid mouse diversity panel, a set of over a hundred inbred strains of mice. In this project, the strains were challenged with Isoproterenol, a beta-adrenergic agonist to induce cardiac hypertrophy and failure. Results are useful for the analysis of heart-related traits in mice
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
208 Samples
Download data: TXT
Series
Accession:
GSE48760
ID:
200048760
20.

Effect of cardiomyocyte-specific deletion of Gch1 on gene expression

(Submitter supplied) To investigate the physiological role of BH4 in cardiac function, we developed mice with cardiomyocyte-specific deletion of (cm)Gch1, the gene that encodes for GTPCH, which responsible for de novo synthesis of BH4. We performed RNA sequencing in heart tissues from cmGch1 KO and WT mice.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
12 Samples
Download data: TXT, XLSX
Series
Accession:
GSE206063
ID:
200206063
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