GEO Logo
   NCBI > GEO > Accession DisplayHelp Not logged in | LoginHelp
GEO help: Mouse over screen elements for information.
Series GSE131296 Query DataSets for GSE131296
Status Public on May 16, 2019
Title Changes in m6A RNA methylation contribute to heart failure progression by modulating translation
Organisms Homo sapiens; Mus musculus
Experiment type Other
Summary We analysed m6A RNA methylation via next generation sequencing (NGS). We found that approximately one quarter of the transcripts in the healthy mouse and human heart exhibit m6A RNA-methylation. There was a mild positive correlation of m6A RNA-methylation at the 5’UTR and coding region with transcript level while m6A RNA-methylation at the 3’UTR showed a mild negative correlation. When we analyzed heart failure in mice and humans we observed that changes in m6A RNA-methylation exceed changes in gene-expression. In mouse and human heart failure transcripts with altered m6A RNA-methylation were mainly linked to metabolic and regulatory pathways while changes in transcript level mainly represented changes in structural plasticity. Mechanistically we could link m6A RNA-methylation to altered RNA translation and protein production. Furthermore, mice with a cardiomyocyte restricted knockout of the demethylase Fto show an impaired function compared to control mice. Thus, we describe for the first time m6A RNA methylation at the genome-wide level in the human heart and in addition use mouse models to provide evidence that changes in m6A RNA-methylation play an important role in heart failure development by affecting regulatory pathways distinct from those genes with altered expression levels regulate. Our data suggest that modulation of epitranscriptomic processes such as m6A-methylation might be an interesting target for therapeutic interventions.
Overall design We analyzed m6A RNA methylation via next generation sequencing (NGS) in mouse models for heart hypertrophy and heart failure along with human failed heart samples. Moreover, we show that methylation levels in heart failure is positively associated with polysome occupancy and thus with translation
Contributor(s) Berulava T, Buchholz E, Ellerdashvilli V, Jain G, Pena T, Fischer A, Toischer K
Citation missing Has this study been published? Please login to update or notify GEO.
Submission date May 15, 2019
Last update date May 18, 2019
Contact name Gaurav Jain
Phone +49-551-39-61194
Organization name The German Center for Neurodegenerative Diseases (German: Deutsches Zentrum für Neurodegenerative Erkrankungen DZNE)
Street address Von-Siebold-Str. 3a, Office no: 2.212
City Göttingen
State/province Lower Saxony
ZIP/Postal code 37075
Country Germany
Platforms (2)
GPL11154 Illumina HiSeq 2000 (Homo sapiens)
GPL13112 Illumina HiSeq 2000 (Mus musculus)
Samples (80)
GSM3768839 DCM564 input
GSM3768840 DCM564 IP
GSM3768841 DCM589 input
BioProject PRJNA543140
SRA SRP198542

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE131296_RAW.tar 15.5 Mb (http)(custom) TAR (of TXT)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap