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In vitro cardiac differentiation is analogous to its in vivo counterpart

ABSTRACT: In vitro cardiac differentiation is analogous to its in vivo counterpart

PROVIDER: PRJNA728745 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14491950.fastq.gz	Fastqsanger.gz
	SRR14491951.fastq.gz	Fastqsanger.gz
	SRR14491952.fastq.gz	Fastqsanger.gz
	SRR14491953.fastq.gz	Fastqsanger.gz
	SRR14491954.fastq.gz	Fastqsanger.gz

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In vitro cardiac differentiation is analogous to its in vivo counterpart

Project description:In vitro cardiac differentiation can be readily achieved in human induced pluripotent stem cells (hiPSCs) via temporal modulation of Wnt signalling. However, its differentiation trajectory and the in vivo counterpart of intermediate progenitor populations has yet to be elucidated. This study aims to capture the most diverse amount of distinct cell populations during in vitro cardiac differentiation by performing single cell RNA-sequencing at day 2, 4, 5 and 9 cells undergoing in vitro cardiac differentiation. Our study has revealed in vitro cardiac differentiation is analogous with in vivo second heart field cell specification.

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Chemical Enhancement of Direct Cardiac Reprogramming In Vitro and In Vivo

Project description:Chemical Enhancement of Direct Cardiac Reprogramming In Vitro and In Vivo

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Chemical Enhancement of Direct Cardiac Reprogramming In Vitro and In Vivo

Project description:Reprogramming of cardiac fibroblasts into induced cardiomyocyte-like cells (iCMs) in situ represents a promising strategy for cardiac regeneration. A combination of three cardiac transcription factors, Gata4, Mef2c and Tbx5 (GMT), can convert fibroblasts into iCMs, albeit with low efficiency in vitro. Here, we screened 5,500 compounds in primary cardiac fibroblasts and found that a combination of the transforming growth factor (TGF)-β inhibitor SB431542 and the WNT inhibitor XAV939 increased reprogramming efficiency eight-fold when added to GMT-overexpressing cardiac fibroblasts. The small-molecules also enhanced the speed and the quality of cell conversion, as we observed beating cells as early as 1 week after reprogramming compared to 6–8 weeks with GMT alone. In vivo, mice exposed to GMT, SB431542, and XAV939 for 2 weeks after myocardial infarction showed significantly improved reprogramming and cardiac function compared to those exposed to only GMT. Human cardiac reprogramming was similarly enhanced upon TGF-b and WNT inhibition and was achieved most efficiently with GMT plus Myocardin. Thus, TGF-β and WNT inhibitors jointly enhance GMT-induced direct cardiac reprogramming from cardiac fibroblasts in vitro and in vivo and provide a more robust platform for cardiac regeneration.

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Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction [Array]

Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in vitro and in vivo in acute MI. Here we show that in vivo cardiac reprogramming generated iCMs from resident CFs, improved cardiac function, and reversed fibrosis in chronic MI using a novel transgenic mouse system. Transcriptome analysis revealed that in vivo cardiac reprogramming altered the interstitial cell landscape, suppressed signs of fibrosis and inflammation, and activated the angiogenic program. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.

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Direct in vivo cardiac reprogramming improves cardiac function and ventricular remodeling in chronic MI.

Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in acute and chronic MI. Here we show that in vivo cardiac reprogramming improved cardiac function, and reversed cardiac remodeling in chronic MI using a novel transgenic mouse system. Transcriptome analysis revealed that in vivo cardiac reprogramming suppressed signs of fibrosis and inflammation. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.

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Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction [scRNA-Seq]

Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in vitro and in vivo in acute MI. Here we show that in vivo cardiac reprogramming generated iCMs from resident CFs, improved cardiac function, and reversed fibrosis in chronic MI using a novel transgenic mouse system. Single-cell transcriptome analysis revealed that cardiac reprogramming shifted matrix-producing CFs, matrifibrocytes, to a quiescent state and changed the interstitial cell landscape, suppressing fibrotic and inflammatory signatures and activating angiogenic program. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.

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Project description:Adult Cardiac hypoxia as a crucial pathogenesis factor can induce detrimental effects on cardiac injury and dysfunction. The global transcriptome and translatome reflecting the cellular response to hypoxia have not yet been extensively studied in myocardium. In this study, adult rats were subjected to acute normobaric hypoxia at 10% oxygen with 10 min (mild hypoxia) and 30 min (severe hypoxia). Rat H9C2 cardiomyocytes were treated with the culture condition (1% O2, 94% N2, and 5% CO2) for mild hypoxia (8 hr) and severe hypoxia(24 hr). We then conducted RNA-seq and Ribo-seq in non-infarcted left ventricular myocardial tissues and H9C2 cells exposed to different periods of hypoxia stress in vivo and in vitro.

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Direct in vivo cardiac reprogramming improves cardiac function and ventricular remodeling in chronic MI.

Project description:Direct in vivo cardiac reprogramming improves cardiac function and ventricular remodeling in chronic MI.

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Robust Cardiac Reprogramming Systems with Selectivity to Cardiac Fibroblasts

Project description:Direct cardiac reprogramming to induce cardiomyocyte-like cells, e.g. by GMT (Gata4, Mef2c and Tbx5), is a promising route for regenerating damaged heart in vivo and disease modeling in vitro. Supplementation with additional factors and chemical agents can enhance efficiency but raises concerns regarding selectivity to cardiac fibroblasts and complicates delivery for in situ cardiac reprogramming. Here, we screened 2000 chemicals with known biological activities and found that a combination of 2C (SB431542 and Baricitinib) significantly enhances cardiac reprogramming by GMT. Without Gata4, MT (Mef2c and Tbx5) plus 2C could selectively reprogram cardiac fibroblasts with enhanced efficiency, kinetics and cardiomyocyte function. More importantly, 2C+MYOCD selectively reprograms human cardiac fibroblasts into cardiomyocyte-like cells. 2C enhances cardiac reprogramming by inhibiting Alk5, Tyk2 and downregulating Oas2, Oas3, Serpina3n and Tgfbi. 2C thus enables selective and robust cardiac reprogramming that can greatly facilitate disease modeling in vitro and advance clinical therapeutic heart regeneration in vivo.

2023-12-13 | GSE213021 | GEO

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