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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE197298 | GEO | 2022/02/26

REPOSITORIES: GEO

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [mRNA-seq]

Project description:The purpose of the study was to compare epicardial transcript abundance between control and Hdac3 knockout (KO) epicardial cells (MEC).

2022-02-26 | GSE197297 | GEO

Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [miRNA-seq]

Project description:We report the application of small-RNA sequencing for high-throughput profiling in mouse epicardial cell (MCEC).

2022-02-26 | GSE197296 | GEO

Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

Project description:Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [mRNA-seq]

Project description:Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [mRNA-seq]

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Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [miRNA-seq]

Project description:Epicardial Hdac3 promotes myocardial growth through a novel microRNA pathway [miRNA-seq]

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Insulin-Like Growth Factor 1 Receptor-Dependent Pathway Drives Epicardial Adipose Tissue Formation After Myocardial Injury.

Project description:BACKGROUND:Epicardial adipose tissue volume and coronary artery disease are strongly associated, even after accounting for overall body mass. Despite its pathophysiological significance, the origin and paracrine signaling pathways that regulate epicardial adipose tissue's formation and expansion are unclear. METHODS:We used a novel modified mRNA-based screening approach to probe the effect of individual paracrine factors on epicardial progenitors in the adult heart. RESULTS:Using 2 independent lineage-tracing strategies in murine models, we show that cells originating from the Wt1+ mesothelial lineage, which includes epicardial cells, differentiate into epicardial adipose tissue after myocardial infarction. This differentiation process required Wt1 expression in this lineage and was stimulated by insulin-like growth factor 1 receptor (IGF1R) activation. IGF1R inhibition within this lineage significantly reduced its adipogenic differentiation in the context of exogenous, IGF1-modified mRNA stimulation. Moreover, IGF1R inhibition significantly reduced Wt1 lineage cell differentiation into adipocytes after myocardial infarction. CONCLUSIONS:Our results establish IGF1R signaling as a key pathway that governs epicardial adipose tissue formation in the context of myocardial injury by redirecting the fate of Wt1+ lineage cells. Our study also demonstrates the power of modified mRNA -based paracrine factor library screening to dissect signaling pathways that govern progenitor cell activity in homeostasis and disease.

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Rno-microRNA-30c-5p promotes myocardial ischemia reperfusion injury in rats through activating NF-?B pathway and targeting SIRT1.

Project description:BACKGROUND:This study aimed to investigate the regulatory effect of rno-microRNA-30c-5p (rno-miR-30c-5p) on myocardial ischemia reperfusion (IR) injury in rats and the underlying molecular mechanisms. METHODS:A rat model of myocardial IR injury was established. The infarct size was detected by 2,3,5-triphenyltetrazolium chloride staining. The pathologic changes of myocardial tissues were detected by hematoxylin-eosin staining. The apoptosis of myocardial cells was measured by TUNEL staining and flow cytometry. The mRNA expression of rno-miR-30c-5p and Sirtuin 1 (SIRT1) was detected by quantitative real-time PCR. The levels of IL-1?, IL-6 and TNF-? were detected by enzyme linked immunosorbent assay. The protein expression of Bax, Bcl-2, caspase-3, p-I?B?, I?B?, p-NF-?B p65, NF-?B p65 and SIRT1 was detected by Western blot. The interaction between rno-miR-30c-5p and SIRT1 was predicted by TargetScan, and further identified by dual luciferase reporter gene and RNA immunoprecipitation assay. RESULTS:The myocardial IR injury model was successfully established in rats. IR induced the myocardial injury in rats and increased the expression of rno-miR-30c-5p. Overexpression of rno-miR-30c-5p enhanced the inflammation, promoted the apoptosis, and activated NF-?B pathway in IR myocardial cells. SIRT1 was the target gene of rno-miR-30c-5p. Silencing of SIRT1 reversed the effects of rno-miR-30c-5p inhibitor on the apoptosis and NF-?B pathway in IR myocardial cells. CONCLUSIONS:Rno-miR-30c-5p promoted the myocardial IR injury in rats through activating NF-?B pathway and down-regulating SIRT1.

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Endocardial HDAC3 is required for myocardial trabeculation

Project description:This SuperSeries is composed of the SubSeries listed below.

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TNF-? promotes invasive growth through the MET signaling pathway.

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Novel gene-pathway identification during the development of human epicardial fat through early life

Project description:Studies in rodents and newborn humans, demonstrate the influence of brown adipose tissue (BAT) in temperature control and energy balance, which also has a critical role in the regulation of body weight. Here, we obtained samples of epicardial adipose tissue (EAT) from neonates, infants and children in order to compare the changes in gene expression with age We used microarrays in order to compare changes between gene to gene interactions by applying systems biology molecular analytical approaches.

2016-06-03 | GSE82155 | GEO

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