PUBLICATION
Acute stress is detrimental to heart regeneration in zebrafish
- Authors
- Sallin, P., Jaźwińska, A.
- ID
- ZDB-PUB-160401-6
- Date
- 2016
- Source
- Open Biology 6(3): (Journal)
- Registered Authors
- Jazwinska, Anna
- Keywords
- anxiolytic, cortisol, crowding, infarction, myocardium, non-mammalian model
- MeSH Terms
-
- Animals
- Cell Proliferation
- Heart/physiology*
- Humans
- Hydrocortisone/metabolism
- Insulin-Like Growth Factor I/genetics
- Insulin-Like Growth Factor I/metabolism
- Myocytes, Cardiac/cytology
- Receptor, IGF Type 1/genetics
- Receptor, IGF Type 1/metabolism
- Regeneration*
- Signal Transduction
- Stress, Physiological*
- Transcriptome
- Zebrafish/genetics
- Zebrafish/physiology*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 27030176 Full text @ Open Biol.
Citation
Sallin, P., Jaźwińska, A. (2016) Acute stress is detrimental to heart regeneration in zebrafish. Open Biology. 6(3).
Abstract
Psychological stress is one of the factors associated with human cardiovascular disease. Here, we demonstrate that acute perceived stress impairs the natural capacity of heart regeneration in zebrafish. Beside physical and chemical disturbances, intermittent crowding triggered an increase in cortisol secretion and blocked the replacement of fibrotic tissue with new myocardium. Pharmacological simulation of stress by pulse treatment with dexamethasone/adrenaline reproduced the regeneration failure, while inhibition of the stress response with anxiolytic drugs partially rescued the regenerative process. Impaired heart regeneration in stressed animals was associated with a reduced cardiomyocyte proliferation and with the downregulation of several genes, includingigfbp1b, a modulator of IGF signalling. Notably, daily stress induced a decrease in Igf1r phosphorylation. As cardiomyocyte proliferation was decreased in response to IGF-1 receptor inhibition, we propose that the stress-induced cardiac regenerative failure is partially caused by the attenuation of IGF signalling. These findings indicate that the natural regenerative ability of the zebrafish heart is vulnerable to the systemic paracrine stress response.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping