Embryonic Cardiotoxicity
Embryonic Cardiotoxicity - Related Videos
04:47
Zebrafish Cardiomyopathy Model: Drug-Induced Cardiotoxicity
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2023
This video describes the technique of creating a zebrafish cardiomyopathy model with minimal variations among experimental groups and in the sample, we create zebrafish cardiomyopathy model using the drug doxorubicin.
10:51
A System for ex vivo Culturing of Embryonic Pancreas
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Cited by 24 •
2012
Here, we describe a method for isolation, culture and manipulation of mouse embryonic pancreas. This represents an excellent ex vivo system for studying various aspects of pancreatic development, including morphogenesis, differentiation and growth. Pancreatic bud explants can be cultured for several days and used in a range of different applications, including whole-mount immunofluorescence and live imaging.
11:00
Using Chicken Embryo as a Powerful Tool in Assessment of Developmental Cardiotoxicities
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Cited by 2 •
2021
Chicken embryos, as a classical developmental model, are used in our lab to assess developmental cardiotoxicities following exposure to various environmental contaminants. Exposure methods and morphological/functional assessment methods established are described in this manuscript.
06:23
Immunostaining of Dissected Zebrafish Embryonic Heart
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Cited by 35 •
2012
A rapid way to conduct immunostaining of zebrafish embryonic heart is described. Compared to the whole mount immunostaining approach, this method dramatically increases the penetration of the antibodies, which allows obtaining high resolution images that reveal cellular/subcellular structures in the heart within a much reduced processing time.
09:38
Preparation of Mouse Embryonic Fibroblast Cells Suitable for Culturing Human Embryonic and Induced Pluripotent Stem Cells
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Cited by 170 •
2012
The quality of mouse embryonic fibroblasts (MEFs) is dictated by the right strain of mouse such as CF-1. Pluripotency-supportive MEFs and conditioned media (CM) obtained from these should contain optimal concentrations of Activin A, Gremlin and Tgfβ1 needed for the Activin/Nodal and FGF pathways to co-operatively maintain self-renewal and pluripotency.
FAQs
Exposure-related injury can interfere with cardiac progenitor specification, the process by which precursor cells acquire heart-forming identities. It may also disturb heart tube formation or vascular development, changing how cardiac structures emerge during embryogenesis. These effects connect molecular or cellular disruption with developmental abnormalities and help explain how an exposure can contribute to congenital heart defects.
These mechanisms affect different levels of cardiac development and function. Oxidative stress can damage developing cells, altered ion-channel activity can disturb electrical signaling and rhythm, and disrupted developmental signaling pathways can change tissue formation. Examining these mechanisms helps researchers distinguish structural abnormalities from functional impairment and relate observed cardiac outcomes to the type of exposure.
Assessment can separate changes in cardiac structure, function, and survival. Investigators may examine heart morphology and vascular development, observe beating and rhythm, evaluate contractility, and measure whether cells remain viable. Considering several outcomes is important because an exposure might alter electrical or mechanical activity without producing the same degree of visible structural change.
Researchers study these effects with animal models, embryonic stem cell-derived cardiomyocytes, and organoid or embryo-like systems. Each model provides a different view of developing cardiac biology, from whole-organism developmental responses to behavior in heart-related cells or simplified three-dimensional systems. Together, these approaches support investigation of structural, functional, and cellular responses to chemical, pharmaceutical, or environmental exposures.
A study may record alterations in cardiac morphology, beating behavior, rhythm, contractility, vascular development, and cell survival. These measurements provide complementary evidence: morphology reflects formation of cardiac structures, rhythm and beating indicate electrical or functional disturbance, contractility reflects mechanical performance, and survival reveals cellular injury. The combined pattern strengthens interpretation of developmental effects.
Testing developmental exposures helps identify potential teratogenic hazards, meaning agents that can disrupt embryonic development, before their effects are considered in broader safety decisions. Findings also clarify mechanisms associated with congenital heart defects. By combining model systems with cardiac structure and function measurements, researchers can improve pharmaceutical screening and inform assessment of environmental or prenatal risks.