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Quantitative Proteomic Profiling of Murine Embryonic Heart Development Reveals a Role for the Mevalonate Pathway in Cardiomyocyte Proliferation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE223239 | GEO | 2023/04/07

REPOSITORIES: GEO

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Quantitative Proteomic Profiling of Murine Embryonic Heart Development Reveals a Role for the Mevalonate Pathway in Cardiomyocyte Proliferation [Cardiomyocytes_Statins_RNASeq]

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2023-04-07 | GSE223238 | GEO

Quantitative Proteomic Profiling of Murine Embryonic Heart Development Reveals a Role for the Mevalonate Pathway in Cardiomyocyte Proliferation [Heart_RNAseq]

Project description:Purpose: The goals of this study are to characterize and analyze the emrbyonic heart transcriptome profiling (RNA-seq) at E9.5, E10.5, E12.5, E14.5 and E16.5. Methods: mRNA profiles of E9.5, E10.5, E12.5, E14.5 and E16.5 C57/Bl6 mouse embryonic hearts were generated by deep sequencing, n=3 or 4 for each age, using Illumina HiSeq2500. Results: Using an optimized data analysis workflow, we mapped at least 36 million sequence reads per sample to the mouse genome (build mm10) and identified 17,537 transcripts in the mouse hearts.

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Quantitative Proteomic Profiling of Murine Embryonic Heart Development Reveals a Role for the Mevalonate Pathway in Cardiomyocyte Proliferation

Project description:Quantitative Proteomic Profiling of Murine Embryonic Heart Development Reveals a Role for the Mevalonate Pathway in Cardiomyocyte Proliferation

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Quantitative Proteomic Profiling of Murine Embryonic Heart Development Reveals a Role for the Mevalonate Pathway in Cardiomyocyte Proliferation [Heart_RNAseq]

Project description:Quantitative Proteomic Profiling of Murine Embryonic Heart Development Reveals a Role for the Mevalonate Pathway in Cardiomyocyte Proliferation [Heart_RNAseq]

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Quantitative Proteomic Profiling of Murine Embryonic Heart Development Reveals a Role for the Mevalonate Pathway in Cardiomyocyte Proliferation [Cardiomyocytes_Statins_RNASeq]

Project description:Quantitative Proteomic Profiling of Murine Embryonic Heart Development Reveals a Role for the Mevalonate Pathway in Cardiomyocyte Proliferation [Cardiomyocytes_Statins_RNASeq]

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Quantitative proteomic profiling identifies global protein network dynamics in murine embryonic heart development.

Project description:Defining the mechanisms that govern heart development is essential for identifying the etiology of congenital heart disease. Here, quantitative proteomics was used to measure temporal changes in the proteome at critical stages of murine embryonic heart development. Global temporal profiles of the over 7,300 proteins uncovered signature cardiac protein interaction networks that linked protein dynamics with molecular pathways. Using this integrated dataset, we identified and demonstrated a functional role for the mevalonate pathway in regulating the cell cycle of embryonic cardiomyocytes. Overall, our proteomic datasets are a resource for studying events that regulate embryonic heart development and contribute to congenital heart disease.

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Screening in Human Cardiac Organoids Identifies a Critical Role for the Mevalonate Pathway in Cardiomyocyte Proliferation

Project description:Re-induction of endogenous proliferation is a promising regeneration strategy for post-mitotic organs. For heart regeneration, we recently discovered that dual inhibition of both GSK3 and MST1 is required for proliferation in mature human cardiac organoids1. However, the mechanisms of action are not yet understood. Here, we de-convolute the mitogenic response using proteomics and report that GSK3 inhibition activates a cell cycle network whereas MST1 inhibition drives the mevalonate pathway. Screening of an additional 105 compounds identified a p38 inhibitor, which activated a cell cycle network, as well as an inhibitor of TGFBR, which activated the mevalonate pathway; combinatorial treatment with these two inhibitors also resulted in synergistic cell cycle activation. The mevalonate pathway which was consistently activated under the most robust proliferative conditions, is down-regulated during in vivo maturation when cardiomyocyte regenerative capacity ceases and inhibition of the mevalonate pathway abolished the myocyte proliferative response to mitogens. Taken together, our findings suggest that the mevalonate pathway synergises with mitogenic agents to enable mature cardiomyocytes to re-enter the cell cycle. These findings have important ramifications for development of cardiac regenerative therapeutics.

2019-03-12 | PXD009133 | Pride

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Murine neonatal cardiac B cells promote cardiomyocyte proliferation and heart regeneration.

Project description:The irreversible loss of cardiomyocytes in the adult heart following cardiac injury leads to adverse cardiac remodeling and ventricular dysfunction. However, the role of B cells in cardiomyocyte proliferation and heart regeneration has not been clarified. Here, we found that the neonatal mice with B cell depletion showed markedly reduced cardiomyocyte proliferation, leading to cardiac dysfunction, fibrosis scar formation, and the complete failure of heart regeneration after apical resection. B cell depletion also significantly impaired heart regeneration and cardiac function in neonatal mice following myocardial infarction (MI). However, B cell depletion in adult mice suppressed tissue inflammation, inhibited myocardial fibrosis, and improved cardiac function after MI. Interestingly, B cell depletion partially restricted cardiomyocyte proliferation in adult mice post-MI. Single-cell RNA sequencing showed that cardiac B cells possessed a more powerful ability to inhibit inflammatory responses and enhance angiogenesis in the postnatal day 1 (P1) mice compared with P7 and adult mice. Besides, the proportion of cardioprotective B cell clusters with high expression levels of S100a6 (S100 calcium-binding protein A6) and S100a4 (S100 calcium-binding protein A4) was greatly decreased in adult heart tissues compared with neonatal mice after cardiac damage. Thus, our study discovers that cardiac B cells in neonatal mice are required for cardiomyocyte proliferation and heart regeneration, while adult B cells promote inflammation and impair cardiac function after myocardial injury.

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