E-MTAB-501 - Transcription profiling of mice hearts comparing microRNA-22 overexpression to wildtype

Released on 1 December 2012, last updated on 3 May 2014
Mus musculus
Samples (6)
Array (1)
Protocols (7)
To explore the role of miR-22 in the heart, we generated miR-22 null and transgenic mice. Cardiac transgenic overexpression of miR-22 in vivo led to cardiac hypertrophy that evolved into progressive dilated cardiomyopathy (DCM) in unstressed hearts. We found that miR-22 directly regulates two transcriptional antagonists, purine rich element binding protein B (PURB), a repressor, and serum response factor (SRF), an activator, in the heart. Through these gain- and loss-of-function experiments in mice, we suggest that a primary function of miR-22 is to fine tune the relative expression and activity of these two transcriptional antagonists to influence contractile gene expression, function, growth and adaptation of the heart to stress.
Experiment types
transcription profiling by array, co-expression, genetic modification, in vivo
microRNA-22 is a modulator of cardiac growth, contractility, and compensation to hemodynamic stress in mice. Priyatansh Gurha, Cei Abreu-Goodger, Maricela O. Ramirez, Stijn van Dongen, Yuqing Chen, Nenad Bartonicek, Caifu Chen, Robert J. Kelm Jr., Anton J. Enright, Brendan Lee, Allan Bradley, George E. Taffet, Mark L. Entman, Antony Rodriguez.
microRNA-22 promotes heart failure through coordinate suppression of PPAR/ERR-nuclear hormone receptor transcription. Gurha P, Wang T, Larimore AH, Sassi Y, Abreu-Goodger C, Ramirez MO, Reddy AK, Engelhardt S, Taffet GE, Wehrens XH, Entman ML, Rodriguez A. :e75882 (2013), PMID:24086656
Investigation descriptionE-MTAB-501.idf.txt
Sample and data relationshipE-MTAB-501.sdrf.txt
Processed data (1)E-MTAB-501.processed.1.zip
Array designA-MEXP-933.adf.txt