New tides: using zebrafish to study renal regeneration

McCampbell, Kristen K.; Wingert, Rebecca A.

doi:10.1016/j.trsl.2013.10.003

Cited by 58 publications

(67 citation statements)

References 87 publications

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“…For clcn2b, we could observe at 26-h postfertilization (hpf) staining in the pronephros of the embryo (Fig. 4a-c), in a region corresponding to the proximal convoluted tubule [37]. We performed a double staining with clcnk, expressed in the distal tubule [55], confirming the identity of the pronephric segment where clcn2b is expressed.…”

Section: Whole Embryo In Situ Hybridization Analysissupporting

confidence: 57%

Identification and characterization of the zebrafish ClC-2 chloride channel orthologs

Pérez-Rius

Gaitán‐Peñas

Estévez

et al. 2014

Pflugers Arch - Eur J Physiol

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ClC-2 is a Cl(-) channel that belongs to the CLC family of chloride channel/transport proteins. ClC-2 molecular role is not clear, and Clcn2 knockout mice develop blindness, sterility, and leukodystrophy by unknown reasons. ClC-2 is associated in the brain with the adhesion molecule GlialCAM, which is defective in a type of leukodystrophy, involving ClC-2 in the homeostasis of myelin. To get more insight into the functions of ClC-2, we have identified in this work the three ClC-2 orthologs in zebrafish. clcn2a and clcn2b resulted from the teleost-specific whole genome duplication, while clcn2c arose from a gene duplication from clcn2b. The expression patterns in adult tissues and embryos of zebrafish clcn2 paralogs support their subfunctionalization after the duplications, with clcn2a being enriched in excitable tissues and clcn2c in ionocytes. All three zebrafish clc-2 proteins interact with human GLIALCAM, that is able to target them to cell junctions, as it does with mammalian ClC-2. We could detect clc-2a and clc-2b inward rectified chloride currents with different voltage-dependence and kinetics in Xenopus oocytes, while clc-2c remained inactive. Interestingly, GlialCAM proteins did not modify clc-2b inward rectification. Then, our work extends the repertoire of ClC-2 proteins and provides new tools for structure-function and physiology studies.

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Section: Whole Embryo In Situ Hybridization Analysissupporting

confidence: 57%

Identification and characterization of the zebrafish ClC-2 chloride channel orthologs

Pérez-Rius

Gaitán‐Peñas

Estévez

et al. 2014

Pflugers Arch - Eur J Physiol

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“…Lotus tetragonolobus lectin (LTL) (proximal tubules marker) and Dolichos biflorus agglutinin (DBA; distal tubules and collective ducts marker) were used as markers of nephron segments. 19,20 Kim-1 was expressed on the apical membrane of proximal tubular cells but not distal tubular or collecting duct cells after gentamicin-induced kidney injury ( Figure 3A). The timecourse of expression of kim1 mRNA revealed that kim1-L and kim1-S transcripts in adult zebrafish kidney were upregulated by 2 days postgentamicin injection (dpi), and remained elevated until 8 dpi, after which they decreased to near-normal levels at 12 dpi, while the expression of kim1-Ig or kim3 and kim4 transcripts was not altered by gentamicin administration ( Figure 3B).…”

Section: Identification Of Zebrafish Kim-1 Familymentioning

confidence: 99%

Mammalian Target of Rapamycin Mediates Kidney Injury Molecule 1-Dependent Tubule Injury in a Surrogate Model

Yin¹,

Naini²,

Chen³

et al. 2015

JASN

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Kidney injury molecule 1 (KIM-1), an epithelial phagocytic receptor, is markedly upregulated in the proximal tubule in various forms of acute and chronic kidney injury in humans and many other species. Whereas acute expression of KIM-1 has adaptive anti-inflammatory effects, chronic expression may be maladaptive in mice. Here, we characterized the zebrafish Kim family, consisting of Kim-1, Kim-3, and Kim-4. Kim-1 was markedly upregulated in kidney after gentamicin-induced injury and had conserved phagocytic activity in zebrafish. Both constitutive and tamoxifen-induced expression of Kim-1 in zebrafish kidney tubules resulted in loss of the tubule brush border, reduced GFR, pericardial edema, and increased mortality. Kim-1-induced kidney injury was associated with reduction of growth of adult fish. Kim-1 expression led to activation of the mammalian target of rapamycin (mTOR) pathway, and inhibition of this pathway with rapamycin increased survival. mTOR pathway inhibition in KIM-1-overexpressing transgenic mice also significantly ameliorated serum creatinine level, proteinuria, tubular injury, and kidney inflammation. In conclusion, persistent Kim-1 expression results in chronic kidney damage in zebrafish through a mechanism involving mTOR. This observation predicted the role of the mTOR pathway and the therapeutic efficacy of mTOR-targeted agents in KIM-1-mediated kidney injury and fibrosis in mice, demonstrating the utility of the Kim-1 renal tubule zebrafish models.

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“…Specifically, it would aid in renal developmental studies, to investigate how different molecules affect nephron segmentation 42 and tubulogenesis 43,44 , processes that are only superficially understood at present. Furthermore, microbead implantation has begun to be used to study regeneration processes in zebrafish 29] and could be adapted for use with any number of organ regeneration models, such as following laser ablation of embryonic tissues like the nephron 45 or in conjunction with methods that have been formulated to perform research with the corresponding adult structures [46][47][48][49] . Finally, microbead implantation has the potential to be used in models of human disease, such as cancer 50,51 or tissue degeneration 52,53 .…”

Section: Discussionmentioning

confidence: 99%

Microbead Implantation in the Zebrafish Embryo

Gerlach

Morales

Wingert

2015

JoVE

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The zebrafish has emerged as a valuable genetic model system for the study of developmental biology and disease. Zebrafish share a high degree of genomic conservation, as well as similarities in cellular, molecular, and physiological processes, with other vertebrates including humans. During early ontogeny, zebrafish embryos are optically transparent, allowing researchers to visualize the dynamics of organogenesis using a simple stereomicroscope. Microbead implantation is a method that enables tissue manipulation through the alteration of factors in local environments. This allows researchers to assay the effects of any number of signaling molecules of interest, such as secreted peptides, at specific spatial and temporal points within the developing embryo. Here, we detail a protocol for how to manipulate and implant beads during early zebrafish development.

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New tides: using zebrafish to study renal regeneration

Cited by 58 publications

References 87 publications

Identification and characterization of the zebrafish ClC-2 chloride channel orthologs

Identification and characterization of the zebrafish ClC-2 chloride channel orthologs

Mammalian Target of Rapamycin Mediates Kidney Injury Molecule 1-Dependent Tubule Injury in a Surrogate Model

Microbead Implantation in the Zebrafish Embryo

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