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Epigenetic remodeling during monolayer cell expansion reduces regeneration potential

ABSTRACT: Epigenetic remodeling during monolayer cell expansion reduces regeneration potential

PROVIDER: PRJNA786775 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17154979_1.fastq.gz	Fastqsanger.gz
	SRR17154979_2.fastq.gz	Fastqsanger.gz
	SRR17154980_1.fastq.gz	Fastqsanger.gz
	SRR17154980_2.fastq.gz	Fastqsanger.gz
	SRR17154981_1.fastq.gz	Fastqsanger.gz

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Epigenetic remodeling during monolayer cell expansion reduces regeneration potential

Project description:The purpose of this study was to understand the how the supression of H3K9me3 impacts the phenotype of chondrocytes during a monolayer expansion process which causes chondrocyte dedifferentiation. Therefore, we compared the mRNA expression profiles of chondrocytes isolated from H3K9M (inducible histone H3.3 lysine-to-methionine mutant) and H3WT (inducibly expressed wild-type H3.3) after 16 population doublings.

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Coupled myovascular expansion directs cardiac growth and regeneration

Project description:Purpose: The goal of this experiment is to better understand the molecular mediators of myovascular coupling during growth and injury. Methods: We performed single cell RNA-sequencing (scRNA-Seq) of border zones of cryoinjured murine hearts collected at P7 using the Drop-seq protocol. Results: Together with in situ hybridization data, results from the scRNA-seq data analysis support a dynamic role for myocardial VEGFA to endothelial VEGFR2 signaling as a regulator of the myovascular expansion during growth and regeneration.

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Neural induction (N2B27 monolayer cluture)

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Monolayer cells transcriptome of human embryonic stem cell differentiation

Project description:We examined the toxic effects of environmental pollutants on embryonic stem cell induced monolayer differentiation by RNA sequencing. RNA extraction was performed on monolayer cells exposed to multiple compounds during monolayer differentiation. The toxic effect of the compound on early embryonic development was obtained by analyzing the difference in RNA expression. Our study provides data closer to the toxic effects of human exposure to neonicotinoids, organophosphate esters and synthetic phenolic antioxidants.

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Expansion of the sagittal suture induces proliferation of skeletal stem cells and sustains endogenous calvarial bone regeneration

Project description:In newborn humans, and up to approximately 2 y of age, calvarial bone defects can naturally regenerate. This remarkable regeneration potential is also found in newborn mice and is absent in adult mice. Since previous studies showed that the mouse calvarial sutures are reservoirs of calvarial skeletal stem cells (cSSCs), which are the cells responsible for calvarial bone regeneration, here we hypothesized that the regenerative potential of the newborn mouse calvaria is due to a significant amount of cSSCs present in the newborn expanding sutures. Thus, we tested whether such regenerative potential can be reverse engineered in adult mice by artificially inducing an increase of the cSSCs resident within the adult calvarial sutures.First, we analyzed the cellular composition of the calvarial sutures in newborn and in older mice, up to 14-mo-old mice, showing that the sutures of the younger mice are enriched in cSSCs. Then, we demonstrated that a controlled mechanical expansion of the functionally closed sagittal sutures of adult mice induces a significant increase of the cSSCs. Finally, we showed that if a calvarial critical size bone defect is created simultaneously to the mechanical expansion of the sagittal suture, it fully regenerates without the need for additional therapeutic aids. Using a genetic blockade system, we further demonstrate that this endogenous regeneration is mediated by the canonical Wnt signaling.This study shows that controlled mechanical forces can harness the cSSCs and induce calvarial bone regeneration. Similar harnessing strategies may be used to develop novel and more effective bone regeneration autotherapies.

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Absent expansion of Axin2 hepatocytes and altered physiology in Axin2CreERT2 mice challenges the role of pericentral hepatocytes in regeneration

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Proteomic analysis of extracellular matrix remodeling during zebrafish heart regeneration

Project description:Adult zebrafish, in contrast to mammals, are able to regenerate their hearts in response to injury or experimental amputation. Our understanding of the cellular and molecular bases that underlie this process, although fragmentary, has increased significantly over the last years. However, the role of the extracellular matrix (ECM) during zebrafish heart regeneration has been comparatively rarely explored. Here, we set out to characterize the ECM protein composition in adult zebrafish hearts, and whether it changed during the regenerative response. For this purpose, we first established a decellularization protocol of adult zebrafish ventricles that significantly enriched the yield of ECM proteins. We then performed proteomic analyses of decellularized control hearts and at different times of regeneration. Our results show a dynamic change in ECM protein composition, most evident at the earliest (7 days post-amputation) time-point analyzed. Regeneration associated with sharp increases in specific ECM proteins, and with an overall decrease in collagens and cytoskeletal proteins. We finally tested by atomic force microscopy that the changes in ECM composition translated to decreased ECM stiffness. Our cumulative results identify changes in the protein composition and mechanical properties of the zebrafish heart ECM during regeneration.

2019-08-26 | PXD010092 | Pride

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