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Transcriptome profiling of neonatal rat ventricular cardiomyocytes overexpressing NFYa or NFE2L1

ABSTRACT: Transcriptome profiling of neonatal rat ventricular cardiomyocytes overexpressing NFYa or NFE2L1

PROVIDER: PRJNA596868 | ENA |

REPOSITORIES: ENA

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Comparison of neonatal and adult rat ventricular cardiomyocytes

Project description:We addressed the question of which protein kinases are expressed in cardiomyocytes. We assessed the changes during postnatal development, comparing profiles in rat neonatal ventricular cardiomyocytes (NVMs) with adult ventricular cardiomyocytes (AVMs). Neonatal and adult rat ventricular cardiomyocytes prepared according to established procedures (Marshall et al. PLoS ONE 2010 5(4):e10027; Fuller and Sugden, FEBs Lett. 1989 247:209-12; Rodrigues and Severson In Biochemical Techniques in the Heart (McNeill, J. H., Ed.) pp 101-115, CRC Press, New York.). mRNA expression profiles compared using Affymetrix rat genome 230 2.0 arrays.

2015-01-01 | E-MTAB-2832 | biostudies-arrayexpress

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Project description:Study on changes in gene expression in primary cultures of neonatal rat ventricular cardiomyocytes to electric stimulation. Through comparing non-stimulated, stimulated and blebbistatin supplemented and stimulated cultures we set out to identify the genes that are specifically activated by electric pulsing separate from cardiomyocyte contractions. After initial recovery phase, primary cultures of neonatal rat ventricular cardiomyocytes were cultured for 3 days without pulsing, with electric pulsing or with electric pulsing combined with blebbistatin. Per treatment: 3 arrays, with samples obtained from 3 separate series of cardiomyocyte isolation and culturing. Per array: sample prepared from pooled (1:1) RNA from duplicate experiments.

2009-12-10 | E-GEOD-15856 | biostudies-arrayexpress

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Transcriptome profiling of neonatal rat ventricular cardiomyocytes overexpressing NFYa or NFE2L1

Project description:The adult mammalian heart is incapable of regeneration following injury. In contrast, the neonatal mouse heart has a transient ability to regenerate, however the molecular mechanism that mediates this regenerative response is not fully understood. Here, by single-nucleus RNA sequencing we map the transcriptome landscape of cardiomyocytes in neonatal mouse hearts at healthy, regenerative, and remodeling conditions. We show that an immature cardiomyocyte population enters cell-cycle in response to injury. Absence of this cardiomyocyte population overtime is associated with the loss of the ability of the heart to regenerate. We show a defined injury response in these cardiomyocytes, including activation of transcription factors NFYa and NFE2L1, which play proliferative and protective roles, respectively. We further show that overexpression of these two factors in vivo promotes heart regeneration. Thus, these findings refined our understanding of cellular basis of neonatal heart regeneration and reveal dynamic transcriptome landscape of cardiomyocytes in response to injury.

2020-03-18 | GSE142364 | GEO

Effect of HectD3 overexpression on gene expression in neonatal rat cardiomyocytes

Project description:The present study focuses on the identification of the gene expression profile of neonatal rat cardiomyocytes (NRVCMs) after overexpressing HectD3, an E3 ligase, through Illumina RNA-sequencing.

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RNA sequencing analysis for differentially expressed genes in neonatal rat cardiomyocytes following knockdown of transcription factor Vezf1

Project description:We performed a set of sequencing experiments to identify the targets of Vascular endothelial zinc finger 1 (Vezf1) in neonatal rat cardiomyocytes. We compared a set of control samples to samples transfected with Vezf1 siRNA by high throughput sequencing. Vascular endothelial zinc finger 1 (Vezf1) siRNA was transfected into the neonatal rat ventricular cardiomyocytes for 24h and thereafter the cells were incubated in serum free medium for 48h.

2019-11-30 | E-MTAB-7124 | biostudies-arrayexpress

RNA-seq of neonatal mouse ventricular cardiomyocytes treated with novel chemical inhibitor

Project description:This experiment investigated the effects of the novel bromodomain inhibitor 3i-1248 in neonatal mouse ventricular cardiomyocytes with and without neurohormonal stimulation with ET-1.

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