Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from pooled biological replicates (n=6) from MEF2D knockdown in neonatal rat ventricular myocytes (NRVMs)

ABSTRACT: Differentiation and maintenance of cardiac muscle is a complex biological process. MEF2D appears to play an important role in the regulation of cardiomyocyte homeostasis. We knocked down expression of MEF2D in NRVMs, and assessed global expression pattern changes in MEF2D knockdown against a negative control. NRVMs were extracted from 1 to 2 day old rat pups and were allowed to recover for 24 hours before being transduced with shRNA viral vectors to knockdown expression of MEF2D or LacZ (negative control). After 3 days, total RNA was harvested for Affymetrix global gene expression microarray analysis. Each array was pooled RNA from six biological replicates.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Adam Gower

PROVIDER: E-GEOD-72157 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MEF2D deficiency in neonatal cardiomyocytes triggers cell cycle re-entry and programmed cell death in vitro.

Estrella Nelsa L NL Clark Amanda L AL Desjardins Cody A CA Nocco Sarah E SE Naya Francisco J FJ

The Journal of biological chemistry 20150820 40

The cardiomyocyte cell cycle is a poorly understood process. Mammalian cardiomyocytes permanently withdraw from the cell cycle shortly after birth but can re-enter the cell cycle and proliferate when subjected to injury within a brief temporal window in the neonatal period. Thus, investigating the mechanisms of cell cycle regulation in neonatal cardiomyocytes may provide critical insight into the molecular events that prevent adult myocytes from proliferating in response to injury or stress. MEF ...[more]

PMID: 26294766

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Dataset Information

Expression data from pooled biological replicates (n=6) from MEF2D knockdown in neonatal rat ventricular myocytes (NRVMs)

Publications

MEF2D deficiency in neonatal cardiomyocytes triggers cell cycle re-entry and programmed cell death in vitro.

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