PUBLICATION
Excessive inflammation impairs heart regeneration in zebrafish breakdance mutant after cryoinjury
- Authors
- Xu, S., Liu, C., Xie, F., Tian, L., Manno, S.H., Manno, F.A.M., Fallah, S., Pelster, B., Tse, G., Cheng, S.H.
- ID
- ZDB-PUB-190402-2
- Date
- 2019
- Source
- Fish & shellfish immunology 89: 117-126 (Journal)
- Registered Authors
- Cheng, Shuk Han, Pelster, Bernd
- Keywords
- Apoptosis, Arrhythmia, Excessive inflammation, Heart regeneration, Immune therapy
- MeSH Terms
-
- Animals
- Cold Temperature/adverse effects
- Disease Models, Animal
- Down-Regulation*
- Heart
- Heart Injuries/etiology
- Heart Injuries/physiopathology*
- Inflammation/etiology
- Inflammation/physiopathology*
- Regeneration*
- Zebrafish/physiology*
- PubMed
- 30928664 Full text @ Fish Shellfish Immunol.
Citation
Xu, S., Liu, C., Xie, F., Tian, L., Manno, S.H., Manno, F.A.M., Fallah, S., Pelster, B., Tse, G., Cheng, S.H. (2019) Excessive inflammation impairs heart regeneration in zebrafish breakdance mutant after cryoinjury. Fish & shellfish immunology. 89:117-126.
Abstract
Inflammation plays a crucial role in cardiac regeneration. Numerous advantages, including a robust regenerative ability, make the zebrafish a popular model to study cardiovascular diseases. The zebrafish breakdance (bre) mutant shares several key features with human long QT syndrome that predisposes to ventricular arrhythmias and sudden death. However, how inflammatory response and tissue regeneration following cardiac damage occur in bre mutant is unknown. Here, we have found that inflammatory response related genes were markedly expressed in the injured heart and excessive leukocyte accumulation occurred in the injured area of the bre mutant zebrafish. Furthermore, bre mutant zebrafish exhibited aberrant apoptosis and impaired heart regenerative ability after ventricular cryoinjury. Mild dosages of anti-inflammatory or prokinetic drugs protected regenerative cells from undergoing aberrant apoptosis and promoted heart regeneration in bre mutant zebrafish. We propose that immune or prokinetic therapy could be a potential therapeutic regimen for patients with genetic long QT syndrome who suffers from myocardial infarction.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping