Evaluation of cardiac dysfunction in adult zebrafish using high frequency echocardiography

Fang, Yuehui; Sun, Yanqing; Luo, Chen; Gu, Junjie; Shi, Zhicai; Li, Guoping; Silvestre, Jean‐Sébastien; Chen, Zhenyue

doi:10.1016/j.lfs.2020.117732

Cited by 14 publications

(10 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Zebrafish in each group were anaesthetized in 0.16 mg/mL tricaine solution for 2 min and placed with the ventral side up in a small sponge holder. Echocardiography was then performed using a VisualSonics Vevo 2100 System echocardiograph (VisualSonics, Toronto, CA, United States) as described previously (Fang et al, 2020).…”

Section: Echocardiographymentioning

confidence: 99%

Identification of Potentially Relevant Genes for Excessive Exercise-Induced Pathological Cardiac Hypertrophy in Zebrafish

et al. 2020

View full text Add to dashboard Cite

Exercise-induced cardiac remodeling has aroused public concern for some time, as sudden cardiac death is known to occur in athletes; however, little is known about the underlying mechanism of exercise-induced cardiac injury. In the present study, we established an excessive exercise-induced pathologic cardiac hypertrophy model in zebrafish with increased myocardial fibrosis, myofibril disassembly, mitochondrial degradation, upregulated expression of the pathological hypertrophy marker genes in the heart, contractile impairment, and cardiopulmonary function impairment. High-throughput RNA-seq analysis revealed that the differentially expressed genes were enriched in the regulation of autophagy, protein folding, and degradation, myofibril development, angiogenesis, metabolic reprogramming, and insulin and FoxO signaling pathways. FOXO proteins may be the core mediator of the regulatory network needed to promote the pathological response. Further, PPI network analysis showed that pik3c3, gapdh, fbox32, fzr1, ubox5, lmo7a, kctd7, fbxo9, lonrf1l, fbxl4, nhpb2l1b, nhp2, fbl, hsp90aa1.1, snrpd3l, dhx15, mrto4, ruvbl1, hspa8b, and faub are the hub genes that correlate with the pathogenesis of pathological cardiac hypertrophy. The underlying regulatory pathways and cardiac pressure-responsive molecules identified in the present study will provide valuable insights for the supervision and clinical treatment of pathological cardiac hypertrophy induced by excessive exercise.

show abstract

Section: Echocardiographymentioning

confidence: 99%

Identification of Potentially Relevant Genes for Excessive Exercise-Induced Pathological Cardiac Hypertrophy in Zebrafish

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Zebrafish were sedated in 0.015% tricaine and immobilized on a sponge immersed in fish water. Imaging was performed on the short axis (perpendicular to the fish) and the long axis (parallel to the fish) using B-mode using the Vevo 2100 and 3100 Cardiac Package, taking the average measurement of three consecutive contractions as described earlier 28 .…”

Section: Methodsmentioning

confidence: 99%

Conditional, tissue-specific CRISPR/Cas9 vector system in zebrafish reveal the role of neuropilin-1b in heart regeneration

Mukhopadhyay

Angom

Wang

et al. 2023

Preprint

View full text Add to dashboard Cite

CRISPR/Cas9 technology-mediated genome editing has significantly improved the targeted inactivation of genes in vitro and in vivo in many organisms. In this study, we have reported a novel CRISPR-based vector system for conditional tissue-specific gene ablation in zebrafish. Specifically, the cardiac-specific cardiac myosins light chain 2 (cmlc2) promoter drives Cas9 expression to silence the neuropilin-1(nrp1) gene in cardiomyocytes in a heat-shock inducible manner. This vector system establishes a unique tool to regulate the gene knockout in both the developmental and adult stages and hence, widens the possibility of loss-of-function studies in zebrafish at different stages of development and adulthood. Using this approach, we investigated the role of neuropilin isoforms nrp1a and nrp1b in response to cardiac injury and regeneration in adult zebrafish hearts. We observed that both the isoforms (nrp1a and nrp1b) are upregulated after the cryoinjury. Interestingly, the nrp1b-knockout significantly altered heart regeneration and impaired cardiac function in the adult zebrafish, demonstrated by reduced heart rate (ECG), ejection fractions, and fractional shortening. In addition, we show that the knockdown of nrp1b but not nrp1a induces activation of the cardiac remodeling genes in response to cryoinjury. To our knowledge, this is the first study where we have reported a heat shock-mediated conditional knockdown of nrp1a and nrp1b isoforms using CRISPR/Cas9 technology in the cardiomyocyte in zebrafish, and furthermore have identified a crucial role for nrp1b isoform in zebrafish cardiac remodeling and eventually heart function in response to injury.

show abstract

“…These efforts to standardize measurements, and establish baseline variation in ECG parameters, allow more detailed analysis of how arrhythmia develops in the aging animal, in genetic models of arrhythmia, or upon inhibition of the parasympathetic nervous system (Yan et al, 2020). Cardiac contractility in embryos and adults can be captured and quantified via echocardiography (Denvir et al, 2008; Fang et al, 2020; Wang et al, 2017), whereas cardiac performance is also indirectly measured through exercise tolerance using swim tunnels, where adult zebrafish undergo timed swims against a current with increasing flow rate, and time to exhaustion is recorded.…”

Section: Cardiac Disease Modelsmentioning

confidence: 99%

Zebrafish as a tractable model of human cardiovascular disease

Bowley

Kugler

Wilkinson

et al. 2021

British J Pharmacology

View full text Add to dashboard Cite

Mammalian models including non-human primates, pigs and rodents have been used extensively to study the mechanisms of cardiovascular disease. However, there is an increasing desire for alternative model systems that provide excellent scientific value while replacing or reducing the use of mammals. Here we review the use of zebrafish, Danio rerio, to study cardiovascular development and disease. The anatomy and physiology of zebrafish and mammalian cardiovascular systems are compared, and we describe the use of zebrafish models in studying the mechanisms of cardiac (e.g. congenital heart defects, cardiomyopathy, conduction disorders, regeneration) and vascular (endothelial dysfunction and atherosclerosis, lipid metabolism, vascular ageing, neurovascular physiology and stroke) pathologies. We also review the use of zebrafish for studying pharmacological responses to cardiovascular drugs, and describe several features of zebrafish that make them a compelling model for in vivo screening of compounds for the treatment cardiovascular disease.

show abstract

Evaluation of cardiac dysfunction in adult zebrafish using high frequency echocardiography

Cited by 14 publications

References 18 publications

Identification of Potentially Relevant Genes for Excessive Exercise-Induced Pathological Cardiac Hypertrophy in Zebrafish

Identification of Potentially Relevant Genes for Excessive Exercise-Induced Pathological Cardiac Hypertrophy in Zebrafish

Conditional, tissue-specific CRISPR/Cas9 vector system in zebrafish reveal the role of neuropilin-1b in heart regeneration

Zebrafish as a tractable model of human cardiovascular disease

Contact Info

Product

Resources

About