PUBLICATION
Loss of Caveolin-1 and caveolae leads to increased cardiac cell stiffness and functional decline of the adult zebrafish heart
- Authors
- Grivas, D., González-Rajal, Á., Guerrero Rodríguez, C., Garcia, R., de la Pompa, J.L.
- ID
- ZDB-PUB-200801-5
- Date
- 2020
- Source
- Scientific Reports 10: 12816 (Journal)
- Registered Authors
- de la Pompa, José Luis, Grivas, Dimitrios
- Keywords
- none
- MeSH Terms
-
- Animals
- Cardiovascular Physiological Phenomena/genetics*
- Caveolae*
- Caveolin 1/genetics*
- Caveolin 1/physiology*
- Elasticity*
- Gene Deletion*
- Myocytes, Cardiac/pathology*
- Myocytes, Cardiac/physiology*
- Signal Transduction/physiology
- Zebrafish*
- PubMed
- 32733088 Full text @ Sci. Rep.
Citation
Grivas, D., González-Rajal, Á., Guerrero Rodríguez, C., Garcia, R., de la Pompa, J.L. (2020) Loss of Caveolin-1 and caveolae leads to increased cardiac cell stiffness and functional decline of the adult zebrafish heart. Scientific Reports. 10:12816.
Abstract
Caveolin-1 is the main structural protein of caveolae, small membrane invaginations involved in signal transduction and mechanoprotection. Here, we generated cav1-KO zebrafish lacking Cav1 and caveolae, and investigated the impact of this loss on adult heart function and response to cryoinjury. We found that cardiac function was impaired in adult cav1-KO fish, which showed a significantly decreased ejection fraction and heart rate. Using atomic force microscopy, we detected an increase in the stiffness of epicardial cells and cells of the cortical zone lacking Cav1/caveolae. This loss of cardiac elasticity might explain the decreased cardiac contraction and function. Surprisingly, cav1-KO mutants were able to regenerate their heart after a cryoinjury but showed a transient decrease in cardiomyocyte proliferation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping