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Gene expression profiles in the heart tissues of heart-specific Bmal1 knockout mice

ABSTRACT: Mice without cardiac Bmal1 function develop severe progressive heart failure with age. To examine the mechanism underlying the failing heart phenotype observed in heart-specific Bmal1 knockout mice, microarray analyses were performed. The analyses revealed that broad classes of genes regulating cellular energy metabolism were upregulated or downregulated in the heart tissues of heart-specific Bmal1 knockout mice compared with those of control animals.

ORGANISM(S): Mus musculus

PROVIDER: GSE61787 | GEO | 2014/09/27

SECONDARY ACCESSION(S): PRJNA262134

REPOSITORIES: GEO

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Project description:Circadian clocks are cell autonomous timekeeping mechanisms that govern critical biological processes. Regarding the heart, the cardiomyocyte circadian clock regulates a diverse array of processes, ranging from transcription and translation, to signaling, metabolism, electrophysiology, and contractility. The importance of this mechanism is underscored by observations that genetic disruption of the cardiomyocyte circadian clock in murine models leads to adverse cardiac remodeling, heart failure, and reduced lifespan. However, the precise molecular links between the cardiomyocyte circadian clock and cardiac physiology/pathology have not been characterized fully. Given that recent studies have highlighted that small RNA species (such as miRNAs) influence both cardiac physiology and pathology, we sought to determine the extent to which cardiomyocyte circadian clock disruption impacts cardiac small RNA species. Accordingly, hearts were collected from cardiomyocyte-specific Bmal1 knockout (CBK) and littermate control (CON) mice at distinct times of the day. Small RNA-seq revealed 47 differentially expressed miRNA species in CBK hearts (in the absence of significant time-of-day-dependent effects). Subsequent bioinformatic analyses predicted that differentially expressed miRNA species in CBK hearts potentially influence processes such as circadian rhythmicity, cellular signaling, and metabolism. Of the induced miRNAs in CBK hearts, 7 were predicted to be targeted by the transcriptional repressors REV-ERB/ (integral circadian clock components that are directly regulated by BMAL1). Similar to CBK hearts, cardiomyocyte-specific Rev-erb/ double knockout (CM-RevDKO) mouse hearts exhibited increased let-7c-1-3p, miR-23b-5p, miR-139-3p, miR-5123, and miR-7068-3p levels. Importantly, 19 putative targets of these 5 miRNAs were commonly repressed in both CBK and CM-RevDKO heart (of which 16 are targeted by let-7c-1-3p). These observations suggest that disruption of the BMAL1–REV-ERB/ axis in the heart leads to induction of a subset of miRNAs, whose predicted mRNA targets have established functions in biological processes such as metabolism and cellular signaling.

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Gene expression profiles in the heart tissues of heart-specific Bmal1 knockout mice

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