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Regulation of Cell Cycle to Stimulate Adult Cardiomyocyte Proliferation and Cardiac Regeneration

ABSTRACT: Regulation of Cell Cycle to Stimulate Adult Cardiomyocyte Proliferation and Cardiac Regeneration

PROVIDER: PRJNA382875 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5445450.fastq.gz	Fastqsanger.gz
	SRR5445460.fastq.gz	Fastqsanger.gz
	SRR5445470.fastq.gz	Fastqsanger.gz
	SRR5445451.fastq.gz	Fastqsanger.gz
	SRR5445461.fastq.gz	Fastqsanger.gz

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α-Ketoglutarate Promotes Cardiomyocyte Proliferation and Heart Regeneration after Myocardial Infarction

Project description:The neonatal mammalian heart is capable of substantial regeneration following injury through cardiomyocyte proliferation. However, this regenerative capacity is lost by postnatal (P) day 7. How to stimulate the adult cardiomyocyte to re-enter the cell cycle is still unknown. Accumulating evidence suggests that cardiomyocyte proliferation depends on its metabolic state. Due to the tight connection between the tricarboxylic acid cycle (TCA) and cell proliferation, we analyzed the TCA metabolites between P0.5 and P7 mouse hearts and found that α-ketoglutarate (α-KG) ranked first among the decreased metabolites. The intraperitoneal injection of exogenous α-KG extended the window of cardiomyocyte proliferation during heart development and promoted heart regeneration after myocardial infarction (MI) by inducing adult cardiomyocyte proliferation. This was confirmed in Ogdh-siRNA-treated mice with increased α-KG levels. Mechanistically, α-KG activates Jmjd3, a histone lysine demethylase, that decreases H3K27me3 expression and deposition of H3K4me3 at the promoters of cell cycle and structural maturation genes in cardiomyocytes. Our present study shows that α-KG promotes cardiomyocyte proliferation by Jmjd3-dependent demethylation and inactivation of H3K27me3 andH3K4me3, which is a potential therapeutic approach for treating MI and heart failure.

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Murine neonatal cardiac B cells promote cardiomyocyte proliferation and heart regeneration

Project description:Since the proliferative capacity of cardiomyocytes is extremely limited in the adult mammalian hearts, the irreversible loss of cardiomyocytes following cardiac injury markedly reduces cardiac function, leading to cardiac remodeling and heart failure. However, the early neonatal mice have a strong ability in cardiomyocyte proliferation and cardiac regeneration after heart damage such as apical resection. Besides of cardiomyocytes, non-myocytes in heart tissue also play important roles in the regeneration process. Previous studies showed that cardiac macrophages, regulatory T cells and CD4+ T cells are all involved in regulating the myocardial regeneration process. However, the roles of other cardiac immune cells in cardiac regeneration remains to be elucidated. B cells is a prominent immune cell in injured heart; here we discovered the indispensable function of cardiac B cells in improving cardiomyocyte proliferation and heart regeneration in neonatal mice.

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Regulation of Cell Cycle to Stimulate Adult Cardiomyocyte Proliferation and Cardiac Regeneration.

Project description:Human diseases are often caused by loss of somatic cells that are incapable of re-entering the cell cycle for regenerative repair. Here, we report a combination of cell-cycle regulators that induce stable cytokinesis in adult post-mitotic cells. We screened cell-cycle regulators expressed in proliferating fetal cardiomyocytes and found that overexpression of cyclin-dependent kinase 1 (CDK1), CDK4, cyclin B1, and cyclin D1 efficiently induced cell division in post-mitotic mouse, rat, and human cardiomyocytes. Overexpression of the cell-cycle regulators was self-limiting through proteasome-mediated degradation of the protein products. In vivo lineage tracing revealed that 15%-20% of adult cardiomyocytes expressing the four factors underwent stable cell division, with significant improvement in cardiac function after acute or subacute myocardial infarction. Chemical inhibition of Tgf-? and Wee1 made CDK1 and cyclin B dispensable. These findings reveal a discrete combination of genes that can efficiently unlock the proliferative potential in cells that have terminally exited the cell cycle.

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Murine neonatal cardiac B cells promote cardiomyocyte proliferation and heart regeneration

Project description:Murine neonatal cardiac B cells promote cardiomyocyte proliferation and heart regeneration

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Tp53 suppression promotes cardiomyocyte proliferation during zebrafish heart regeneration

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Cardiomyocyte S1pr1 regulates cardiac regeneration via AKT/mTOR signaling pathway

Project description:Mammalian hearts had the capability to regenerate cardiomyocyte and completely recover after heart injury within a limited time window after birth. It has been shown that sphingosine 1-phospahte receptor 1 (S1pr1) was highly expressed in cardiomyocytes and played an important role in heart development and pathological cardiac remodeling. Herein, we aim to investigate the role of CM-S1pr1 for cardiac regeneration and tissue repair after heart injury. We generated cardiomyocyte (CM)-specific S1pr1 knock-out mice and showed that CM-specific S1pr1 loss-of-function significantly severely reduced cardiomyocyte proliferation and heart regeneration in neonatal mice after both apex resection and myocardial infarction, whereas S1pr1 gain-of-function by AAV9-mediated CM-specific overexpression of S1pr1 significantly boosted cardiac regeneration and improved cardiac functions after heart injuries. We next identified that S1pr1 activated AKT/mTOR/CyclinD1 and Bcl-2 signaling pathways, and thus promoted cardiomyocyte proliferation and inhibited CM apoptosis, respectively.Of note, we applied CM-targeted gene therapy by AAV9-cTNT to specifically overexpress S1pr1 in cardiomyocytes and achieved an efficient S1pr1 overexpression in CMs in vivo. This CM-targeted strategy to overexpress S1pr1 significantly enhanced cardiac regeneration and improved cardiac functions after myocardial infarction in an adult mouse model, suggesting a potential strategy to boost adult cardiac regeneration in vivo.

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Regulation of Cell Cycle to Stimulate Adult Cardiomyocyte Proliferation and Cardiac Regeneration

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

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [RNA-seq]

Project description:To identify the potential microRNAs (miRNAs) involved in the regulation of cardiomyocyte (CM) proliferation during homeostasis and injury, RNA sequencing (RNA-seq) in mouse cardiac ventricles was performed on postnatal day 1, 7, and 28 (P1, P7, and P28). Significant upregulation of MiR-128 was found in P7 hearts as compared to P1. To further specify the effect of miR-128 in the heart, RNA-Seq was performed in control mice (Ctrl) and miR-128 overexpression mice (miR-128OE) on P7. These data provide novel insights into the mechanisms by which adult CMs exit the cell cycle arrest and is fundamental for therapeutic manipulation to stimulate endogenous CM proliferate in cardiac regeneration.

2018-01-02 | GSE107678 | GEO

Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [miRNA-seq]

2018-01-02 | GSE107679 | GEO

Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration

Project description:Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration

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