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.
Abstract
To better understand the molecular mechanisms of regeneration and explore the potential signalling pathways as therapeutic targets for heart attacks.
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.
Appropriate activation of MAPK/ERK signalling is essential for zebrafish cardiac regeneration.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping