Effect of Charme lncRNA knockout (KO) in cardiac development [RNA-seq]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE200878 | GEO | 2023/03/18
REPOSITORIES: GEO
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Project description:Effect of Charme lncRNA knockout (KO) in cardiac development [RNA-seq]
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Project description:Cardiac maturation during perinatal transition of heart is critical for functional adaptation to hemodynamic load and nutrient environment. Perturbation in this process has major implications in congenital heart defects (CHDs). Transcriptome programming during perinatal stages is important information but incomplete in current literature, particularly, the expression profiles of the long noncoding RNAs (lncRNAs) are not fully elucidated From comprehensive analysis of transcriptomes derived from neonatal mouse heart left and right ventricles, a total of 45,167 unique transcripts were identified, including 21,916 known and 2,033 novel lncRNAs. Among these lncRNAs, 196 exhibited significant dynamic regulation along maturation process. By implementing parallel weighted gene co-expression network analysis (WGCNA) of mRNA and lncRNA datasets, several lncRNA modules coordinately expressed in a developmental manner similar to protein coding genes, while a few of them revealed chamber specific patterns. Out of 2,442 lncRNAs located within 50 KBs of protein coding genes, 11% significantly correlates with the expression of their neighboring genes. The impact of Ppp1r1b-lncRNA on the corresponding partner gene Tcap was validated in cultured myoblasts. While this concordant regulation was also conserved in human infantile hearts. Furthermore, the Ppp1r1b-lncRNA/Tcap expression ratio was identified as a molecular signature that differentiated CHD phenotypes lncRNA dataset: neonatal mouse heart left and right ventricles
2016-08-20 | E-GEOD-85726 | biostudies-arrayexpress
Project description:MATR3 CLIP-seq analysis on embryonal (E15) murine hearts was performed to identify the protein RNA-interactors during murine cardiac development and to characterize the differential binding of the protein in conditon of KO of the lncRNA Charme.
2023-03-18 | GSE200877 | GEO
Project description:Purpose: To identify the differential TFIIB bindingl patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Methods: Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq. Results: In accordance with previosly published data (Sayed D, et. al. JBC, 2013 Jan 25;288(4):2546-58) with genome wide polII and H3K9ac status during cardiac hypertrophy (GSE50637), Denovo TFIIB recruitment was restricted to speclaized genes with cardiac hypertrophy. Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq.
2014-11-17 | E-GEOD-56813 | biostudies-arrayexpress
Project description:Adult-onset diseases can be associated with in utero events, but mechanisms for such temporally distant dysregulation of organ function remain unknown. The polycomb histone methyltransferase, Ezh2, stabilizes transcription by depositing repressive histone marks during development that persist into adulthood, but the function of Ezh2-mediated transcriptional stability in postnatal organ homeostasis is not understood. Here, we show that Ezh2 stabilizes the postnatal cardiac gene expression program and prevents cardiac pathology, primarily by repressing the homeodomain transcription factor Six1 in differentiating cardiac progenitors. Loss of Ezh2 in embryonic cardiac progenitors, but not in differentiated cardiomyocytes, resulted in postnatal cardiac pathology, including cardiomyocyte hypertrophy and fibrosis. Loss of Ezh2 caused broad derepression of skeletal muscle genes, including the homeodomain transcription factor Six1, which is expressed in cardiac progenitors but is normally silenced upon cardiac differentiation. Many of the deregulated genes are direct Six1 targets, implying a critical requirement for stable repression of Six1 in cardiac myocytes. Indeed, upon de-repression, Six1 promotes cardiac pathology, as it was sufficient to induce cardiac hypertrophy. Furthermore, genetic reduction of Six1 levels almost completely rescued the pathology of Ezh2-deficient hearts. Thus, repression of a single transcription factor in cardiac progenitors by Ezh2 is essential for stability of the adult heart gene expression program and homeostasis. Our results suggest that epigenetic dysregulation during discrete developmental windows can predispose to adult disease and dysregulated stress responses. Global gene expression profiles of Ezh2-deficient hearts. The right ventricle and the interventricular septum of five wild type (Ezh2f/f) and four Ezh2-deficient (Ezh2f/f;Mef2cAHF::Cre) mice were analyzed.
2011-12-31 | E-GEOD-30076 | biostudies-arrayexpress
Project description:Purpose: To identify the differential transcriptional patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Results: Our data revealed novel transcriptional patterns during cardiac growth conditions. The results showed that most of the essential genes are regulated by promoter clearance of paused RNA pol II, while de novo recruitment is required for regulation of mostly speclaized genes during cardiac growth. We have identified two major modes of gene regulation durign cardiac hypertrophy and four transcriptional growth patterns. The results are published in January 2013 issue of Journal of Biological Chemistry. Methods: Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for RNA polII and H3K9ac- ChIP-Seq.
2013-09-06 | E-GEOD-50637 | biostudies-arrayexpress
Project description:lncRNA Cfast knockdown in cardiac fibroblasts
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Project description:Purpose: To identify the differential TFIIB bindingl patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Methods: Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq. Results: In accordance with previosly published data (Sayed D, et. al. JBC, 2013 Jan 25;288(4):2546-58) with genome wide polII and H3K9ac status during cardiac hypertrophy (GSE50637), Denovo TFIIB recruitment was restricted to speclaized genes with cardiac hypertrophy.
2014-11-17 | GSE56813 | GEO
Project description:We deleted Tfr1 in the heart to determine the role of Tfr1 in iron uptake in normal cardiac funciton We used microarrays to identify global gene changes associated with deletion of Tfr1 in skeletal muscle We isolated RNA from WT and Tfr1 KO hearts at both postnatal day 5 and postnatal day 10.RNA was labaled and hibridized to Affymetrics microarrays.
2015-05-12 | E-GEOD-68745 | biostudies-arrayexpress
Project description:Cardiac fibrosis occurs in most cardiac diseases, which reduces cardiac muscle compliance, impairs both systolic and diastolic heart function and, ultimately, leads to heart failure. Using unbiased transcriptome profiling in a mouse model of myocardial infarction, we identified a cardiac-fibroblast enriched lncRNA (AK048087) named cardiac fibroblast-associated transcript (Cfast), which is significantly elevated after myocardial infarction. Here, we show that silencing Cfast expression by lentiviral shRNAs resulted in suppression of fibrosis-related gene expression and transdifferentiation of myofibroblasts into cardiac fibroblasts. We performed the RNA-seq profiling in both lentivirus Cfast knockdown and lentivirus scramble group in cardiac fibroblasts. Finally, the transcriptome analysis indicates that genes related to cell differentiation, cell migration, extracellular matrix organization downregulated in Cfast knockdown group.
2020-11-13 | GSE161389 | GEO