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Transcription profiling of right ventricule from arrhythmogenic heterozygous plakoglobin deficient mice undergone endurance training to identify transcriptional responses to training.


ABSTRACT: Endurance training accelerated development of right ventricular dysfunction and arrhythmias in plakoglobin+/- mice. Histology and electron microscopy did not identify right ventricular abnormalities. To identify differences in the transcriptional response to training gene expression profiling was performed. Experiment Overall Design: Gene expressson analyses were performed in 5 pairs of plakoglobin (+/-) mice and their wildtype littermates. Four pairs of trained mice and one pair of old untrained mice were studied. Training induced expression of several hypertrophy associated genes such as ANP but no differences between the trained plakoglobin (+/-) mice and wt mice was seen.

ORGANISM(S): Mus musculus

DISEASE(S): arrhythmias and right ventricular dysfunction

SUBMITTER: Henning Witt 

PROVIDER: E-GEOD-4120 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Age- and training-dependent development of arrhythmogenic right ventricular cardiomyopathy in heterozygous plakoglobin-deficient mice.

Kirchhof Paulus P   Fabritz Larissa L   Zwiener Melanie M   Witt Henning H   Schäfers Michael M   Zellerhoff Stephan S   Paul Matthias M   Athai Timur T   Hiller Karl-Heinz KH   Baba Hideo A HA   Breithardt Günter G   Ruiz Patricia P   Wichter Thomas T   Levkau Bodo B  

Circulation 20061009 17


<h4>Background</h4>Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disorder that causes sudden death and right ventricular heart failure in the young. Clinical data suggest that competitive sports may provoke ARVC in susceptible persons. Genetically, loss-of-function mutations in desmosomal proteins (plakophilin, desmoplakin, or plakoglobin) have been associated with ARVC. To test the hypothesis that reduced desmosomal protein expression causes ARVC, we studied the cardiac  ...[more]

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