Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA110483 | ENA |
REPOSITORIES: ENA
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Project description:Calcium signaling is a central regulator of cardiomyocyte growth and function. Calmodulin is a critical mediator of calcium signals. Because the amount of calmodulin within cardiomyocytes is limiting, precise regulation of calmodulin expression may be an important for regulation of calcium signaling. In this study, we show for the first time that calmodulin levels are regulated post-transcriptionally in heart failure. The cardiomyocyte-restricted microRNA miR-1 inhibited translation of calmodulin-encoding mRNAs via highly conserved target sites within their 3’-untranslated regions. In keeping with its effect on calmodulin expression, miR-1 downregulated calcium-calmodulin signaling through the calcineurin to NFAT. miR-1 also negatively regulated expression of Mef2a and Gata4, key transcription factors that mediate calcium-dependent changes in gene expression. Consistent with downregulation of these hypertrophy-associated genes, miR-1 attenuated cardiomyocyte hypertrophy in cultured neonatal rat cardiomyocytes and in the intact adult heart. Our data indicate that miR-1 regulates cardiomyocyte growth responses by negatively regulating the calcium-signaling components calmodulin, Mef2a, and Gata4.
2009-03-05 | GSE13874 | GEO
Project description:Calcium signaling is a central regulator of cardiomyocyte growth and function. Calmodulin is a critical mediator of calcium signals. Because the amount of calmodulin within cardiomyocytes is limiting, precise regulation of calmodulin expression may be an important for regulation of calcium signaling. In this study, we show for the first time that calmodulin levels are regulated post-transcriptionally in heart failure. The cardiomyocyte-restricted microRNA miR-1 inhibited translation of calmodulin-encoding mRNAs via highly conserved target sites within their 3â-untranslated regions. In keeping with its effect on calmodulin expression, miR-1 downregulated calcium-calmodulin signaling through the calcineurin to NFAT. miR-1 also negatively regulated expression of Mef2a and Gata4, key transcription factors that mediate calcium-dependent changes in gene expression. Consistent with downregulation of these hypertrophy-associated genes, miR-1 attenuated cardiomyocyte hypertrophy in cultured neonatal rat cardiomyocytes and in the intact adult heart. Our data indicate that miR-1 regulates cardiomyocyte growth responses by negatively regulating the calcium-signaling components calmodulin, Mef2a, and Gata4. We show that miR-1 is downregulated in a murine heart failure model. miRNAs expression changes were measured in calcineurin transgenic model of heart failure and control mice using a Luminex platform. Reduced miR-1 expression was associated with broad alteration in expression of predicted target genes. To test this, we measured miRs including miR-1 and genome wide transcriptome changes in vivo and in vitro system. Calcineurin transgenic heart was compared to nontransgenic heart (NTg vs. CNTg). We also investigated the gene expression changes during the course of cardiomyocytes differentiation using DMSO treated P19CL6 cell lines. Two time points (day 6 and day 10) were compared to identified the gene expression changes of predicted miR-1 targets (Day 6 vs. Day 10).
2010-06-25 | E-GEOD-13874 | biostudies-arrayexpress
Project description:Regulatory factors play important roles in cardiac hypertrophy by regulating gene expression in cardiomyocytes.HSP70, a heat shock protein encoded by HSPA1A ,is induced by hypertrophic stimulation and then causes cardiac hypertrophy. However, the regulation mechanism of HSP70 in cardiac hypertrophy is unknown. In this study, we established the cardiac hypertrophy mouse model to explore the differentially expressed genes and found Hspa1a was significantly increased in treated samples. Then Hspa1a was overexpressed in mouse cardiac HL-1 cells and we analyzed the changes of transcriptome expression by high throughput sequencing. The results showed that HSPA1A selectively regulates the expression of ncRNAs (Rn7sk,Rmrp), negatively regulates the expression of genes involved in inflammatory and immune response, including Cxcl1，Ccl2，Ccl7,Cxcl5, Fas andC3, which were also validated by RT-qPCR experiment. The HSPA1A-regulated genes and ncRNAs are highly associated with cardiac hypertrophy. Alternative splicing analysis revealed HSPA1A preferred to regulate genes enriched in transcriptional regulation, including Asxl2 and Runx1. These results indicate that the heat shock protein-HSPA1A may play a role in the occurrence and development of myocardial hypertrophy by regulating the expression of immune inflammatory response related pathway genes and ncRNAs related to myocardial hypertrophy.
2021-10-06 | GSE158635 | GEO
Project description:Dysregulated deltaNp63alpha negatively regulates p73-mediated maspin expression
| PRJNA150125 | ENA
Project description:Myocyte Enhancer Factor 2 (MEF2) proteins are involved in multiple developmental, physiological, and pathological processes in vertebrates. Protein:protein interactions underlie the plethora of biological processes impacted by MEF2A, necessitating a detailed characterization of the MEF2A interactome. A nanobody based affinity-purification/mass spectrometry strategy was employed to achieve this goal. Specifically, the MEF2A protein complexes were captured from myogenic lysates using a GFP-tagged MEF2A protein immobilized with a GBP-nanobody followed by LC-MS/MS proteomic analysis to identify MEF2A interactors.
2024-02-27 | PXD050042 | Pride
Project description:MicroRNA-34a regulates cardiac ageing and function
| PRJNA186702 | ENA
Project description:LIN-42, the Caenorhabditis elegans PERIOD homolog, negatively regulates microRNA transcription
| PRJNA251425 | ENA
Project description:Purpose: Cardiac hypertrophy is a well-known major risk factor for poor prognosis in patients with cardiovascular diseases. Dysregulation of intracellular Ca2+ is involved in the pathogenesis of cardiac hypertrophy. However, the precise mechanism underlying cardiac hypertrophy remains elusive. Here, we investigated whether pressure-overload induced hypertrophy can be induced by destabilization of cardiac ryanodine receptor (RyR2) through calmodulin (CaM) dissociation and subsequent Ca2+ leakage, and whether it can be genetically rescued by enhancing the binding affinity of CaM to RyR2. Methods: To examine the role of CaM-RyR2 complex in the development of pressure-overload induced cardiac hypertrophy, whole transcriptome analysis using RNA-seq analysis in the hearts from WT and homozygous RyR2V3599K/V3599K (V3599K) mice with or without transverse aortic constriction (TAC) was performed to elucidate the RyR2 signaling pathway in the heart. Results: Gene expression increased in WT (+TAC) hearts compared to WT (-TAC) hearts; however, this increase was not observed in V3599K (+TAC) hearts. Conclusions: Enhanced CaM binding to RyR2 decreased expression of hypertrophy-related genes.
2020-10-07 | GSE158536 | GEO
Project description:RORa regulates developmental and angiotensin II-induced cardiac hypertrophy
| PRJNA386510 | ENA
Project description:Identfification of MEF2A target genes using ChIP-exo in skeletla muscle and primary cardiomyocytes. Identfification of MEF2A target genes using ChIP-exo and RNA-seq in skeletal muscle and primary cardiomyocytes. MEF2 plays a profound role in the regulation of transcription in cardiac and skeletal muscle lineages. To define the overlapping and unique MEF2A genomic targets, we utilized ChIP-exo analysis of cardiomyocytes and skeletal myoblasts. Of the 2783 and 1648 MEF2A binding peaks in skeletal myoblasts and cardiomyocytes, respectively, 294 common binding sites were identified. Genomic targets were compared to differentially expressed genes in RNA-seq analysis of MEF2A depleted myogenic cells.
2014-09-09 | GSE61204 | GEO