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Muscle injury prepares stem cells for terminal myocyte differentiation through changes in gene expression and long-term changes in DNA methylation

ABSTRACT: Muscle injury prepares stem cells for terminal myocyte differentiation through changes in gene expression and long-term changes in DNA methylation

PROVIDER: PRJNA601987 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10704063.fastq.gz	Fastqsanger.gz
	SRR10704064.fastq.gz	Fastqsanger.gz
	SRR10704065.fastq.gz	Fastqsanger.gz
	SRR10704066.fastq.gz	Fastqsanger.gz
	SRR10704067.fastq.gz	Fastqsanger.gz

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Muscle injury causes gene expression changes that are related to long-term changes in stem cell DNA methylation [RNA-Seq]

Project description:Injury to muscle brings about the activation of stem cells, which then generate new myocytes to replace the damaged tissue. We now demonstrate that this activation causes a dramatic change in the stem cell methylation pattern that prepares them epigenetically for terminal myocyte differentiation. These demethylation and de novo methylation events occur at regulatory elements associated with genes involved in myogenesis. Local injury of one muscle brings about an almost identical epigenetic change in satellite cells from other muscles in the body, as well. Furthermore, this same methylation state is also generated in muscle stem cells of female animals following full-term pregnancy, even in the absence of any injury. In all of these cases, which appear to be mediated by circulating factors, the new methylation profile is then stably maintained in resident muscle stem cells and thus represents a molecular memory of previous physiological events that is probably programmed to provide a mechanism for adapting to the environment. Here we show the changes in gene expression that accompany the changes in DNA methylation.

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Muscle injury prepares stem cells for terminal myocyte differentiation through changes in gene expression and long-term changes in DNA methylation

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Project description:Rationale: Neonatal mice have the capacity to regenerate their hearts in response to injury, but this potential is lost after the first week of life. The transcriptional changes that underpin mammalian cardiac regeneration have not been fully characterized at the molecular level. Objective: The objectives of our study were to determine if myocytes revert the transcriptional phenotype to a less differentiated state during regeneration and to systematically interrogate the transcriptional data to identify and validate potential regulators of this process. Methods and Results: We derived a core transcriptional signature of injury-induced cardiac myocyte regeneration in mouse by comparing global transcriptional programs in a dynamic model of in vitro and in vivo cardiac myocyte differentiation, in vitro cardiac myocyte explant model, as well as a neonatal heart resection model. The regenerating mouse heart revealed a transcriptional reversion of cardiac myocyte differentiation processes including reactivation of latent developmental programs similar to those observed during de-stabilization of a mature cardiac myocyte phenotype in the explant model. We identified potential upstream regulators of the core network, including interleukin 13 (IL13), which induced cardiac myocyte cell cycle entry and STAT6/STAT3 signaling in vitro. We demonstrate that STAT3/periostin and STAT6 signaling are critical mediators of IL13 signaling in cardiac myocytes. These downstream signaling molecules are also modulated in the regenerating mouse heart. Conclusions: Our work reveals new insights into the transcriptional regulation of mammalian cardiac regeneration and provides the founding circuitry for identifying potential regulators for stimulating heart regeneration.

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Transcriptional Reversion of Cardiac Myocyte Fate During Mammalian Cardiac Regeneration.

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