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Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome transfer provides a model for understanding the phenotype of cardiomyocytes

ABSTRACT: We show that the transfer of the adult ventricular myocyte (AVM) transcriptome into either a fibroblast or an astrocyte converts the host cell into a cardiomyocyte. Transcriptome-effected cardiomyocytes (tCardiomyocytes) display morphologies, immunocytochemical properties, and expression profiles of postnatal cardiomyocytes. Cell morphology analysis shows that tCardiomyoctes are elongated and have a similar length-to-width ratio as AVMs. These global phenotypic changes occur in a time-dependent manner and confer electroexcitability to the tCardiomyocytes. tCardiomyocyte generation does not require continuous overexpression of specific transcription factors; for example, the expression level of transcription factor Mef2c is higher in tCardiomyocytes than in fibroblasts, but similar in tCardiomyocytes and AVMs. These data highlight the dominant role of the gene expression profile in developing and maintaining cellular phenotype. The transcriptomeinduced phenotype remodeling–generated tCardiomyocyte has significant implications for understanding and modulating cardiac disease development. Transcriptome transfer can change one cell type to another cell type. We transfect cardiomyocyte transciptome into fibroblast and astrocyte. Transcriptomes from single cells are isolated and amplified and then hybridize on Affymetrix array.

ORGANISM(S): Mus musculus

SUBMITTER: Tae Kim

PROVIDER: E-GEOD-30164 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptome transfer provides a model for understanding the phenotype of cardiomyocytes

Project description:We show that the transfer of the adult ventricular myocyte (AVM) transcriptome into either a fibroblast or an astrocyte converts the host cell into a cardiomyocyte. Transcriptome-effected cardiomyocytes (tCardiomyocytes) display morphologies, immunocytochemical properties, and expression profiles of postnatal cardiomyocytes. Cell morphology analysis shows that tCardiomyoctes are elongated and have a similar length-to-width ratio as AVMs. These global phenotypic changes occur in a time-dependent manner and confer electroexcitability to the tCardiomyocytes. tCardiomyocyte generation does not require continuous overexpression of specific transcription factors; for example, the expression level of transcription factor Mef2c is higher in tCardiomyocytes than in fibroblasts, but similar in tCardiomyocytes and AVMs. These data highlight the dominant role of the gene expression profile in developing and maintaining cellular phenotype. The transcriptomeinduced phenotype remodeling–generated tCardiomyocyte has significant implications for understanding and modulating cardiac disease development.

2011-06-23 | GSE30164 | GEO

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Gene expression in mouse heart

Project description:Growth and expansion of ventricular chambers is essential during cardiogenesis and is achieved by proliferation of cardiac progenitors that are not fully differentiated. Disruption of this process can lead to prenatal lethality. In contrast, adult cardiomyocytes achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Moreover, the function of embryonic cardiac fibroblasts, derived from epicardium, and their secreted factors are largely unknown. Using a novel co-culture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. b1 integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of b1 integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation. This SuperSeries is composed of the following subset Series: GSE14411: Gene expression in b1-integrin wild-type and knockout mouse heart GSE14412: Gene expression in mouse embyonic cardiomyocytes, fibroblasts and adult cardiac fibroblasts Refer to individual Series

2009-01-14 | E-GEOD-14414 | biostudies-arrayexpress

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