Understanding copper sensitivity in zebrafish (Danio rerio) through the intracellular localization of copper transporters in a hepatocyte cell-line ZFL and the tissue expression profiles of copper transporters

Leung, King Pong; Chen, Dongshi; Chan, King Ming

doi:10.1039/c3mt00366c

Cited by 25 publications

(12 citation statements)

References 40 publications

(42 reference statements)

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“…However Atp7a may not be essential for Cu transport from the yolk sac or within the embryo (Mendelsohn et al, 2006 ). In adult zebrafish, the expression pattern of Atp7a is similar to that found in mammalian tissues, such as intestine, kidney, heart, gills and liver (Chen and Chan, 2011 ; Leung et al, 2014 ). Atp7a is expressed most abundantly in the kidneys under elevated Cu level as well as under control conditions which suggests a major role of Atp7a in Cu export in D. rerio similar to observations in mice (Leung et al, 2014 ).…”

Section: Other Animal Models Of Menkes Diseasesupporting

confidence: 54%

“…Danio rerio absorbs Cu in two ways: via the intestine similarly to what is observed in mammals, and by the gills. Interestingly, the highest expression of the major Cu importer Ctr1 protein was detected in gut (Leung et al, 2014 ). Furthermore, the expression of Atp7a mRNA is ubiquitous in the zebrafish embryo and starts early in development (Mendelsohn et al, 2006 ).…”

Section: Other Animal Models Of Menkes Diseasementioning

confidence: 99%

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Mottled Mice and Non-Mammalian Models of Menkes Disease

Lenartowicz

Krzeptowski

Lipiński

et al. 2015

Front. Mol. Neurosci.

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Menkes disease is a multi-systemic copper metabolism disorder caused by mutations in the X-linked ATP7A gene and characterized by progressive neurodegeneration and severe connective tissue defects. The ATP7A protein is a copper (Cu)-transporting ATPase expressed in all tissues and plays a critical role in the maintenance of copper homeostasis in cells of the whole body. ATP7A participates in copper absorption in the small intestine and in copper transport to the central nervous system (CNS) across the blood-brain-barrier (BBB) and blood–cerebrospinal fluid barrier (BCSFB). Cu is essential for synaptogenesis and axonal development. In cells, ATP7A participates in the incorporation of copper into Cu-dependent enzymes during the course of its maturation in the secretory pathway. There is a high degree of homology (>80%) between the human ATP7A and murine Atp7a genes. Mice with mutations in the Atp7a gene, called mottled mutants, are well-established and excellent models of Menkes disease. Mottled mutants closely recapitulate the Menkes phenotype and are invaluable for studying Cu-metabolism. They provide useful models for exploring and testing new forms of therapy in Menkes disease. Recently, non-mammalian models of Menkes disease, Drosophila melanogaster and Danio rerio mutants were used in experiments which would be technically difficult to carry out in mammals.

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Section: Other Animal Models Of Menkes Diseasesupporting

confidence: 54%

Section: Other Animal Models Of Menkes Diseasementioning

confidence: 99%

Mottled Mice and Non-Mammalian Models of Menkes Disease

Lenartowicz

Krzeptowski

Lipiński

et al. 2015

Front. Mol. Neurosci.

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“…In fact, CTR1 mRNA is expressed in zebrafish lateral line hair cells (McDermott et al, 2007 ), although, the level of CTR1 protein expression and its functionality has not yet been studied in either zebrafish lateral line or inner ear hair cells. Further, mRNA tissue expression of copper transporter genes can vary significantly between mammals, zebrafish and other fish species after copper exposure (Leung et al, 2014 ). Therefore, mammalian hair cells may respond differently than fish to copper-based compounds.…”

Section: Causes and Mechanisms Of Hair Cell Damagementioning

confidence: 99%

Sensory hair cell death and regeneration in fishes

Monroe

Rajadinakaran

Smith

2015

Front. Cell. Neurosci.

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Sensory hair cells are specialized mechanotransductive receptors required for hearing and vestibular function. Loss of hair cells in humans and other mammals is permanent and causes reduced hearing and balance. In the early 1980’s, it was shown that hair cells continue to be added to the inner ear sensory epithelia in cartilaginous and bony fishes. Soon thereafter, hair cell regeneration was documented in the chick cochlea following acoustic trauma. Since then, research using chick and other avian models has led to great insights into hair cell death and regeneration. However, with the rise of the zebrafish as a model organism for studying disease and developmental processes, there has been an increased interest in studying sensory hair cell death and regeneration in its lateral line and inner ears. Advances derived from studies in zebrafish and other fish species include understanding the effect of ototoxins on hair cells and finding otoprotectants to mitigate ototoxin damage, the role of cellular proliferation vs. direct transdifferentiation during hair cell regeneration, and elucidating cellular pathways involved in the regeneration process. This review will summarize research on hair cell death and regeneration using fish models, indicate the potential strengths and weaknesses of these models, and discuss several emerging areas of future studies.

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“…Several studies have validated the use of zebrafish larvae as a model for cardio-, hepato- and neurotoxicity research1112. Currently, zebrafish larvae or embryos are being used as in vivo platforms to study the toxic effects of nanoparticles1314. Table 1 provides a literature overview of studies on the toxicity of nanomaterials as a function of their physicochemical characteristics using zebrafish models.…”

mentioning

confidence: 99%

Use of Zebrafish Larvae as a Multi-Endpoint Platform to Characterize the Toxicity Profile of Silica Nanoparticles

Pham

Roo

Nguyen

et al. 2016

Sci Rep

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Nanomaterials are being extensively produced and applied in society. Human and environmental exposures are, therefore, inevitable and so increased attention is being given to nanotoxicity. While silica nanoparticles (NP) are one of the top five nanomaterials found in consumer and biomedical products, their toxicity profile is poorly characterized. In this study, we investigated the toxicity of silica nanoparticles with diameters 20, 50 and 80 nm using an in vivo zebrafish platform that analyzes multiple endpoints related to developmental, cardio-, hepato-, and neurotoxicity. Results show that except for an acceleration in hatching time and alterations in the behavior of zebrafish embryos/larvae, silica NPs did not elicit any developmental defects, nor any cardio- and hepatotoxicity. The behavioral alterations were consistent for both embryonic photomotor and larval locomotor response and were dependent on the concentration and the size of silica NPs. As embryos and larvae exhibited a normal touch response and early hatching did not affect larval locomotor response, the behavior changes observed are most likely the consequence of modified neuroactivity. Overall, our results suggest that silica NPs do not cause any developmental, cardio- or hepatotoxicity, but they pose a potential risk for the neurobehavioral system.

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Understanding copper sensitivity in zebrafish (Danio rerio) through the intracellular localization of copper transporters in a hepatocyte cell-line ZFL and the tissue expression profiles of copper transporters

Cited by 25 publications

References 40 publications

Mottled Mice and Non-Mammalian Models of Menkes Disease

Mottled Mice and Non-Mammalian Models of Menkes Disease

Sensory hair cell death and regeneration in fishes

Use of Zebrafish Larvae as a Multi-Endpoint Platform to Characterize the Toxicity Profile of Silica Nanoparticles

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