Systemic hypertension increases cardiac workload and subsequently induces signaling networks in heart that underlie myocyte growth (hypertrophic response) through expansion of sarcomeres with the aim to increase contractility. However, conditions of increased workload can induce both adaptive and maladaptive growth of heart muscle. Previous studies implicate two members of the AP-1 transcription factor family, junD and fra-1, in regulation of heart growth during hypertrophic response. In this study, we investigate the function of the AP-1 transcription factors, c-jun and c-fos, in heart growth. Using pressure overload-induced cardiac hypertrophy in mice and targeted deletion of Jun or Fos in cardiomyocytes, we show that c-jun is required for adaptive cardiac hyphertrophy, while c-fos is dispensable in this context. c-jun promotes expression of sarcomere proteins and suppresses expression of extracellular matrix proteins. Capacity of cardiac muscle to contract depends on organization of principal thick and thin filaments, myosin and actin, within the sarcomere. In line with decreased expression of sarcomere-associated proteins, Jun-deficient cardiomyocytes present disarrangement of filaments in sarcomeres and actin cytoskeleton disorganization. Moreover, Jun-deficient hearts subjected to pressure overload display pronounced fibrosis and increased myocyte apoptosis finally resulting in dilated cardiomyopathy. In conclusion, c-jun but not c-fos is required to induce a transcriptional program aimed at adapting heart growth upon increased workload.
The AP-1 transcription factor c-Jun prevents stress-imposed maladaptive remodeling of the heart.
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Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
Age, Specimen part
View SamplesThe mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart.
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
Age, Specimen part
View SamplesThe mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions, 4 biological replicates per condition
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
No sample metadata fields
View SamplesThe mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart.
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
Specimen part
View SamplesThe mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions, 3 biological replicates per condition
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
Age, Specimen part, Cell line, Subject
View SamplesExpression profiles at various time points after surgical intervention for pressure-overload induced cardiac hypertrophy and failure.
Small proline-rich protein 1A is a gp130 pathway- and stress-inducible cardioprotective protein.
Sex, Age, Specimen part, Disease, Disease stage, Subject
View SamplesExponentially growing cells and type II persister cells from the DS1-(hipQ)-strain
Novel protocol for persister cells isolation.
Specimen part, Disease, Cell line
View SamplesPURPOSE
Gene expression profiling reveals novel biomarkers in nonsmall cell lung cancer.
Specimen part, Disease
View SamplesTo identify potential targets of miR-34a, we performed transcriptional profiling on proneural TS543 GBM cells, focusing on mRNAs whose levels decreased in response to miR-34a transfection as compared to control oligonucleotide.
miR-34a repression in proneural malignant gliomas upregulates expression of its target PDGFRA and promotes tumorigenesis.
Cell line, Treatment
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