PUBLICATION
Zebrafish integrin a3b is required for cardiac contractility and cardiomyocyte proliferation
- Authors
- Yu, H.L., Hwang, S.L.
- ID
- ZDB-PUB-220206-3
- Date
- 2022
- Source
- Biochemical and Biophysical Research Communications 595: 89-95 (Journal)
- Registered Authors
- Hwang, Sheng-Ping L.
- Keywords
- Cardiac contractility, Cardiomyocyte proliferation, Itga3b, Z-disc, Zebrafish
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Apoptosis/genetics
- Cell Proliferation/genetics
- Gene Knockdown Techniques
- Green Fluorescent Proteins/genetics
- Green Fluorescent Proteins/metabolism
- In Situ Hybridization
- Integrin alpha3/genetics*
- Integrin alpha3/metabolism
- Microscopy, Electron, Transmission
- Mutation
- Myocardial Contraction/genetics
- Myocardium/cytology
- Myocardium/metabolism*
- Myocytes, Cardiac/cytology
- Myocytes, Cardiac/metabolism*
- Myocytes, Cardiac/ultrastructure
- Sarcolemma/metabolism
- Sarcolemma/ultrastructure
- Sarcomeres/metabolism
- Zebrafish/genetics*
- Zebrafish/metabolism
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 35121232 Full text @ Biochem. Biophys. Res. Commun.
Citation
Yu, H.L., Hwang, S.L. (2022) Zebrafish integrin a3b is required for cardiac contractility and cardiomyocyte proliferation. Biochemical and Biophysical Research Communications. 595:89-95.
Abstract
In cardiac muscle cells, heterodimeric integrin transmembrane receptors are known to serve as mechanotransducers, translating mechanical force to biochemical signaling. However, the roles of many individual integrins have still not been delineated. In this report, we demonstrate that Itga3b is localized to the sarcolemma of cardiomyocytes from 24 to 96 hpf. We further show that heterozygous and homozygous itga3b/bdf mutant embryos display a cardiomyopathy phenotype, with decreased cardiac contractility and reduced cardiomyocyte number. Correspondingly, proliferation of ventricular and atrial cardiomyoctyes and ventricular epicardial cells is decreased in itga3b mutant hearts. The contractile dysfunction of itga3b mutants can be attributed to cardiomyocyte sarcomeric disorganization, including thin myofilaments with blurred and shortened Z-discs. Together, our results reveal that Itga3b localizes to the myocardium sarcolemma, and it is required for cardiac contractility and cardiomyocyte proliferation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping