PUBLICATION
P66Shc (Shc1) Zebrafish Mutant Line as a Platform for Testing Decreased Reactive Oxygen Species in Pathology
- Authors
- Haslem, L., Hays, J.M., Zhang, X.A., Hays, F.A.
- ID
- ZDB-PUB-221115-5
- Date
- 2022
- Source
- Journal of cardiovascular development and disease 9(11): (Journal)
- Registered Authors
- Keywords
- ROS, ShcA, apoptosis, ischemia/reperfusion, mitochondrial dysfunction, myocardial infarction, p66Shc, zebrafish
- MeSH Terms
- none
- PubMed
- 36354784 Full text @ J Cardiovasc Dev Dis
Citation
Haslem, L., Hays, J.M., Zhang, X.A., Hays, F.A. (2022) P66Shc (Shc1) Zebrafish Mutant Line as a Platform for Testing Decreased Reactive Oxygen Species in Pathology. Journal of cardiovascular development and disease. 9(11):.
Abstract
Reactive oxygen species (ROS) dysregulation exacerbates many pathologies but must remain within normal ranges to maintain cell function. Since ROS-mediated pathology and routine cell function are coupled, in vivo models evaluating low-ROS background effects on pathology are limited. Some models alter enzymatic antioxidant expression/activity, while others involve small molecule antioxidant administration. These models cause non-specific ROS neutralization, decreasing both beneficial and detrimental ROS. This is detrimental in cardiovascular pathology, despite the negative effects excessive ROS has on these pathologies. Thus, current trends in ROS-mediated pathology have shifted toward selective inhibition of ROS producers that are dysregulated during pathological insults, such as p66Shc. In this study, we evaluated a zebrafish heterozygote p66Shc hypomorphic mutant line as a low-ROS myocardial infarction (MI) pathology model that mimics mammalian MI. Our findings suggest this zebrafish line does not have an associated negative phenotype, but has decreased body mass and tissue ROS levels that confer protection against ROS-mediated pathology. Therefore, this line may provide a low-ROS background leading to new insights into disease.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping