PUBLICATION
MAPK/ERK signalling is required for zebrafish cardiac regeneration
- Authors
- Liu, P., Zhong, T.P.
- ID
- ZDB-PUB-170330-2
- Date
- 2017
- Source
- Biotechnology Letters 39(7): 1069-1077 (Journal)
- Registered Authors
- Zhong, Tao P.
- Keywords
- Cardiac regeneration, MAPK/ERK signalling, MEK, Zebrafish, pERK
- MeSH Terms
-
- Animals
- Benzimidazoles/administration & dosage
- Heart/physiology*
- Mitogen-Activated Protein Kinase Kinases/metabolism*
- Protein Kinase Inhibitors/administration & dosage
- Regeneration*
- Signal Transduction*
- Zebrafish/physiology*
- PubMed
- 28353145 Full text @ Biotechnol. Lett.
Citation
Liu, P., Zhong, T.P. (2017) MAPK/ERK signalling is required for zebrafish cardiac regeneration. Biotechnology Letters. 39(7):1069-1077.
Abstract
Objectives To better understand the molecular mechanisms of regeneration and explore the potential signalling pathways as therapeutic targets for heart attacks.
Results After treatment with the MEK inhibitor AZD6244 upon cardiac injury, the core members in MAPK/ERK signalling-mek and erk-demonstrate elevated expression, and these proteins are deposited at the injury site in zebrafish. pERK is also induced in non-cardiomyocytes near the injury site. Furthermore, the induced expression of a dominant-negative form of MEK1 inhibits zebrafish cardiac regeneration, characterized by increased cardiac fibrosis (a hallmark of regenerative failure), reduced or delayed production of regenerative myocardium, and migration of FLI1+ endothelial cells, without direct inhibition of cardiomyocyte proliferation.
Conclusion Appropriate activation of MAPK/ERK signalling is essential for zebrafish cardiac regeneration.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping