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Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Visium]

ABSTRACT: Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Visium]

PROVIDER: PRJNA974494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24673361.fastq.gz	Fastqsanger.gz
	SRR24673362.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Visium]

Project description:Cardiomyocytes are highly metabolic cells responsible for generating the contractile force that drives heart function. During fetal development and regeneration, these cells undergo active division but lose their proliferation activity in the adult heart. The mechanisms that coordinate their metabolism and proliferation are not fully understood. Here, we study the developmental functions of the transcription factor NFYa, which we previously identified from regenerating cardiomyocytes. We show that loss of NFYa profoundly alters cardiomyocyte composition, with a decrease in immature regenerative cells and an increase in trabecular and mature cardiomyocytes, as revealed by spatial and single-cell transcriptome analyses. NFYa-deleted cardiomyocytes exhibited reduced proliferation and impaired mitochondrial metabolism, contributing to the cardiac growth defect. NFYa acts as a transcriptional activator of mitochondrial metabolic genes as well as cell-cycle genes in cardiomyocytes through its interaction with the cofactor SP2, providing a direct link between metabolism and proliferation at the gene transcriptional level. Our study reveals a key role of NFYa in regulating cardiac growth before birth and a previously unrecognized transcriptional control mechanism of metabolic genes in the heart, and highlights the importance of mitochondrial metabolism during fetal heart development and regeneration.

2023-10-13 | GSE232962 | GEO

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Multiome]

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Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [ChIP-seq]

2023-10-13 | GSE232960 | GEO

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development

Project description:Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development

| PRJNA974492 | ENA

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Multiome]

Project description:Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Multiome]

| PRJNA974493 | ENA

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [ChIP-seq]

Project description:Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [ChIP-seq]

| PRJNA974488 | ENA

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development

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

2023-10-13 | GSE232963 | GEO

FOXK1 and FOXK2 Promote Cardiomyocyte Proliferation and Heart Regeneration

Project description:Promoting the proliferation of endogenous cardiomyocytes represents a promising strategy for treating cardiac injuries. Identifying key factors that regulate cardiomyocyte proliferation can advance the development of novel therapies for heart regeneration. Here we identify that FOXK1 and FOXK2 act as master regulators of cardiomyocyte proliferation and metabolism. The expression of FOXK1 and FOXK2 decreased with postnatal heart development. Cardiomyocyte-specific knockout of Foxk1 or Foxk2 inhibited neonatal heart regeneration after myocardial infarction (MI) injury. Conversely, AAV9-mediated cardiomyocyte-specific overexpression of FOXK1 or FOXK2 prolonged the postnatal proliferative window of cardiomyocytes and enhanced cardiac repair in adult mice by promoting endogenous cardiomyocyte proliferation after MI. Mechanistically, FOXK1 and FOXK2 induce Ccnb1 and Cdk1 transcription and cardiomyocyte cell cycle progression, respectively. Ccnb1 knockdown hindered FOXK1 overexpression-induced cardiomyocyte proliferation, and the same effect was observed when Cdk1 was knocked down in FOXK2 overexpressing cardiomyocytes. Additionally, we further revealed that FOXK1 and FOXK2 induced a metabolic shift toward glycolysis by promoting HIF1α expression in cardiomyocytes, which favors cardiomyocyte proliferation. Our findings identify FOXK1 and FOXK2 as critical triggers of cardiomyocyte proliferation and define these two transcription factors as novel therapeutic targets for myocardial infarction.

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A high-resolution single-cell multiomic atlas of the human fetal lung - Visium

Project description:Fetal lung samples at 12–20 post conception week (pcw) from the HDBR, up to 0.5cm3 in size, were embedded in OCT and flash-frozen in dry-ice cooled isopentane. Twelve-micron cryosections were cut onto Visium slides, haematoxylin and eosin stained and imaged at 20X magnification on a Hamamatsu Nanozoomer 2.0 HT Brightfield. These were then further processed according to the 10X Genomics Visium protocol, using a permeabilization time of 18 min for 12–17 pcw samples and 24 min for 19 pcw and older samples. Images were exported as tiled tiffs for analysis. Dual-indexed libraries were prepared as in the 10X Genomics protocol, pooled at 2.25 nM and sequenced in 4 samples per Illumina Novaseq SP flow cell with read lengths of 28 bp for R1, 10 bp for i7 index, 10 bp for i5 index, 90 bp for R2.

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Prrx1b restricts fibrosis and promotes Nrg1-dependent cardiomyocyte proliferation during zebrafish heart regeneration

Project description:Fibroblasts are activated to repair the heart following injury. Fibroblast activation in the mammalian heart leads to a permanent fibrotic scar that impairs cardiac function. In other organisms, such as zebrafish, cardiac injury is followed by transient fibrosis and scar-free regeneration. The mechanisms that drive scarring versus scar-free regeneration are not well understood. Here, we show that the homeobox-containing transcription factor Prrx1b is required for scar-free regeneration of the zebrafish heart as the loss of Prrx1b results in excessive fibrosis and impaired cardiomyocyte proliferation. Through lineage tracing and single-cell RNA sequencing we find that Prrx1b is activated in epicardial-derived cells where it restricts TGFβ ligand expression and collagen production. Furthermore, through combined in vitro experiments in human fetal epicardial-derived cells and in vivo rescue experiments in zebrafish, we conclude that Prrx1 stimulates Nrg1 expression and promotes cardiomyocyte proliferation. Collectively, these results indicate that Prrx1 is a key transcription factor that balances fibrosis and regeneration in the injured zebrafish heart.

2021-09-16 | GSE153170 | GEO

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