Key result
Zebrafish reporter accurately models pathological nppb gene induction and distinct responses to Trichostatin A and U0126.
Why the study?
It has been challenging to find novel chemical or genetic modifiers of cardiomyocyte hypertrophy and heart failure pathways using traditional cell-based or mammalian models.
Can an in vivo zebrafish natriuretic peptide reporter assay identify chemical modifiers of hypertrophic cardiomyopathy signaling?
Population
Developing zebrafish embryonic hearts
Comparison
Chemical agents including Trichostatin A vs U0126 in hypertrophic cardiomyopathy model
Design
In vivo luciferase-based transgenic reporter assay in zebrafish
Authors
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Offers zebrafish platform for screening HCM modulators; leaves open human translation.
Can an in vivo zebrafish natriuretic peptide reporter assay identify chemical modifiers of hypertrophic cardiomyopathy signaling?
A novel in vivo zebrafish reporter assay successfully models pathological induction of natriuretic peptides and identifies chemical modifiers of hypertrophic cardiomyopathy signaling.
Becker et al. (2011) studied Hypertrophic cardiomyopathy and heart failure. Trichostatin A and U0126 was evaluated on Pathological induction patterns of the zebrafish nppb gene. A zebrafish luciferase-based transgenic reporter line accurately modeled pathological induction of the nppb gene and demonstrated distinct responses to Trichostatin A and U0126.
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