PUBLICATION
Block the function of nonmuscle myosin II by blebbistatin induces zebrafish embryo cardia bifida
- Authors
- Wang, X., Chong, M., Wang, X., Wang, H., Zhang, J., Xu, H., Zhang, J., Liu, D.
- ID
- ZDB-PUB-141119-4
- Date
- 2015
- Source
- In vitro cellular & developmental biology. Animal 51(3): 211-7 (Journal)
- Registered Authors
- Xu, Hui
- Keywords
- none
- MeSH Terms
-
- Animals
- Animals, Newborn
- Carrier Proteins/metabolism
- Cell Shape/drug effects
- Dose-Response Relationship, Drug
- Embryo, Nonmammalian/abnormalities*
- Embryo, Nonmammalian/drug effects*
- Embryo, Nonmammalian/pathology
- Fertilization
- Heart Defects, Congenital/embryology*
- Heart Defects, Congenital/pathology
- Heterocyclic Compounds, 4 or More Rings/pharmacology*
- Membrane Proteins/metabolism
- Mice
- Myocytes, Cardiac/drug effects
- Myocytes, Cardiac/pathology
- Myosin Type II/antagonists & inhibitors*
- Myosin Type II/metabolism
- Zebrafish/embryology*
- Zebrafish Proteins/metabolism
- PubMed
- 25403653 Full text @ In Vitro Cell Dev. Biol. Anim.
Citation
Wang, X., Chong, M., Wang, X., Wang, H., Zhang, J., Xu, H., Zhang, J., Liu, D. (2015) Block the function of nonmuscle myosin II by blebbistatin induces zebrafish embryo cardia bifida. In vitro cellular & developmental biology. Animal. 51(3):211-7.
Abstract
Nonmuscle myosin II (NM II) is the name given to the multi-subunit protein product of three genes encoding different nonmuscle myosin heavy chains including NM II-A, NM II-B, and NM II-C. Blebbistatin is a small molecule that has been shown to be a relatively specific inhibitor of NM II. Blocking the function of NM II by blebbistatin induces zebrafish embryo cardia bifida at a dose-dependent manner. In situ hybridization analysis with ventricular marker ventricular myosin heavy chain (vmhc) and atrial marker atrial myosin heavy chain (amhc) showed each of the heart contained both distinct atria and ventricle. However, the cardia bifida embryos had highly variable distance between two separate ventricles. We also provided evidence that time window from 12 to 20 h post fertilization (hpf) is necessary and sufficient for cardia bifida formation caused by blebbistatin treatment. Expression of spinster homolog 2 (spns2) was decreased in blebbistatin-treated embryos, suggesting the cardia bifida phenotype caused by NM II inhibition was relevant to precardiac mesoderm migration defects. Through in situ hybridization analysis, we showed that foxa1 was expressed in endoderm of blebbistatin-treated embryos at 24-hpf stage, suggesting the endoderm formation is normal in cardia bifida embryos caused by blebbistatin treatment. In addition, we demonstrated that blebbistatin treatment resulted in morphology alteration of zebrafish cardiomyocytes in vivo and neonatal mouse cardiomyocytes in vitro.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping