GSE125596
Transcriptome-wide profiling of thyroid hormone-dependent gene expression in the mouse heart
During the first weeks after birth, cardiomyocytes within the mouse heart progressively exit the cell cycle, binucleate, and lose regenerative capacity.  We have determined that postnatal day 14 (P14) mouse hearts incapable of responding to thryoid hormone signaling have enhanced proliferation, retain greater populations of mononucleated cardiomyocytes, and show increased regenerative ability. In this study, we perform transcriptome-wide analysis to identify gene networks regulating thryoid hormone-dependent exit of cardiomyocyte cell-cycle and loss of regenerative potential. Overall design: Transgenic mice possessing cardiomyocyte-specific expression of Cre recombinase (Myh6-Cre) were bred with knock-in mice harboring an allele with Cre-dependent expression of a dominant negative mutant form of thryoid hormone receptor alpha (TRalphaAMI).  Three Myh6-Cre; TRalphaAMI pups and three TRalphaAMI littermate control pups were raised to postnatal day 14 (P14), total RNA was extracted from their hearts, and RNA-seq was performed to identify differentially expressed genes.