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Novel targets of microRNA miR-142 in cardiac myocytes

ABSTRACT: The nuclear acetyltransferase p300 is a dose-dependent and limiting regulator of cardiac hypertrophy. p300 regulates hypertrophy by controlling the expression of specific microRNAs.The objective of this study was to dissect the role of miR-142 during p300 regulated hypertophic growth in vitro and in vivo and to verify its targets.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE31121 | GEO | 2012/03/07

SECONDARY ACCESSION(S): PRJNA144955

REPOSITORIES: GEO

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Novel targets of microRNA miR-142 in cardiac myocytes

Project description:The nuclear acetyltransferase p300 is a dose-dependent and limiting regulator of cardiac hypertrophy. p300 regulates hypertrophy by controlling the expression of specific microRNAs.The objective of this study was to dissect the role of miR-142 during p300 regulated hypertophic growth in vitro and in vivo and to verify its targets. MiR142 and a non target control were overexpressed using lentivirus in primary culture of neonatal cardiac myocytes. Overexpression was checked 48 hour post transfection. Samples include miR142 OE and non target from three different experiments.

2012-03-07 | E-GEOD-31121 | biostudies-arrayexpress

Yuan- microRNAs upregulated in Ep300-overexpressing mouse heart

Project description:Objective: To characterize downstream effectors of p300 acetyltransferase in the myocardium. Background: Acetyltransferase p300 is a central driver of the hypertrophic response to increased workload, but its biological targets and downstream effectors are incompletely known. Methods and Results: Mice expressing a myocyte-restricted transgene encoding acetyltransferase p300, previously shown to develop spontaneous hypertrophy, were observed to undergo robust compensatory blood vessel growth together with increased angiogenic gene expression. Chromatin immunoprecipitation demonstrated binding of p300 to the enhancers of the angiogenic regulators Angpt1 and Egln3. Interestingly, p300 overexpression in vivo was also associated with relative upregulation of several members of the anti-angiogenic miR-17~92 cluster in vivo. Confirming this finding, both miR-17-3p and miR-20a were upregulated in neonatal rat ventricular myocytes following adenoviral transduction of p300. Relative expression of most members of the 17~92 cluster was similar in all 4 cardiac chambers and in other organs, however, significant downregulation of miR-17-3p and miR-20a occurred between 1 and 8 months of age in both wt and tg mice. The decline in expression of these microRNAs was associated with increased expression of VEGFA, a validated miR-20a target. In addition, miR-20a was demonstrated to directly repress p300 expression through a consensus binding site in the p300 3’UTR. In vivo transduction of p300 resulted in repression both of p300 and of p300-induced angiogenic transcripts. Conclusion: p300 drives an angiogenic transcription program during hypertrophy that is fine-tuned in part through direct repression of p300 by miR-20a. 4 littermates, 3 transgene-expressing and 1 wild-type were analyzed. Samples were spotted in duplicate.

2013-09-30 | E-GEOD-50843 | biostudies-arrayexpress

Effects of silencing miR-142-3p on the pathological and physiological functions of cardiac fibroblasts

Project description:MicroRNAs (miRs), a group of small and non-coding RNAs, negatively regulate gene expression via promoting messenger RNA (mRNA) degradation or blocking mRNA translation. Many miRs have been recognized as biomarkers or possible targets for the diagnosis or therapy of some diseases. Among them, miR-142-3p was involved in the occurrences and progression of various cardiovascular diseases. Previous studies found that miR-142-3p upregulation could ameliorate myocardial ischemia/reperfusion (I/R)-induced transdifferentiation of fibroblasts to myofibroblasts and collagen deposition. miR-142-3p-mediacted autophagy was reported as a novel mechanism towards I/R-induced cardiac injure. Besides, miR-142-3p could mitigate myocardial mitochondrial dysfunction. Thus, it is worth studying whether silencing miR-142-3p may affect the pathological and physiological functions of cardiac fibroblasts.

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Gene profiling changes in BM Lin-Sca-1+c-Kit+ cells (LSKs) from miR-142-/- (KO), miR-142+/+ (WT), miR-142-/- BCR-ABL (BC CML) and miR-142+/+ BCR-ABL (CP CML) mice. [bulk RNA-Seq]

Project description:To gain insight into how miR-142 deficit drives a BC-like transformation, we performed RNA-seq on bone marrow (BM) Lin-Sca-1+c-Kit+ cells (LSKs) harvested from normal miR-142+/+ (wt) and miR-142−/− (miR-142 KO) mice, as well as from leukemic miR-142+/+ BCR-ABL (CP CML) and miR-142−/− BCR-ABL (BC CML) mice, two weeks after BCR-ABL induction. We then performed gene expression profiling analysis using data obtained from RNA-seq of 24 samples of LSK cells from 4 mouse strains (KO vs WT, KO CML vs CML).

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Yuan- microRNAs upregulated in Ep300-overexpressing mouse heart

2013-09-30 | GSE50843 | GEO

Expression data for effect of p300 knockdown and Doxorubicin treatment in cardiac myocytes

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Expression profiling of miR-142 deficient Treg cells

Project description:miR-142 gene is specifically and abundantly expressed in hematopoietic lineages. Mice with specific deletion of this miRNA gene in Treg develop fatal autoimmunity. We used RNA-seq to detect whole transcriptome changes in miR-142 null Treg cells.

2021-12-07 | GSE190192 | GEO

Epression profiling of miR-142 deficient CD19+ B cells

Project description:miR-142 gene is specifically and abundantly expressed in hematopoietic cells. Mice that lack this miRNA gene develop immunodeficiency and display altered hematopoeisis. We used microarrays to detect whole transcriptome changes in miR-142 null B cells.

2015-06-15 | GSE61919 | GEO

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