Claudin tight junction proteins in rainbow trout ( Oncorhynchus mykiss ) skin: Spatial response to elevated cortisol levels

Gauberg, Julia; Kolosov, Dennis; Kelly, Scott P.

doi:10.1016/j.ygcen.2016.10.006

Cited by 11 publications

(20 citation statements)

References 55 publications

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“…For example, corticosterone levels are reported to rise during stress and inflammatory responses in amphibians (Rollins-Smith, 2017), and specifically in L. caerulea infected with Bd (Peterson et al, 2013). Corticosteroids have been shown to alter mRNA and protein abundance of Ocln (Chasiotis and Kelly, 2011;Förster et al, 2005), Tric (Kolosov and Kelly, 2013), Cldns (Kielgast et al, 2016;Kobayashi et al, 2016;Gauberg et al, 2017;Kolosov and Kelly, 2017;Kolosov et al, 2017b) and ZO-1 (Singer et al, 1994; Chasiotis and Kelly, 2011) in various vertebrate models. Therefore, increased systemic levels of corticosterone in L. caerulea that would occur with infection may have triggered an en masse increase in TJ protein transcript abundance.…”

Section: All Examined Tj Protein Transcripts Increase In Abundance Wimentioning

confidence: 99%

A lethal fungal pathogen directly alters tight junction proteins in the skin of a susceptible amphibian

Gauberg

Cramp

et al. 2018

Journal of Experimental Biology

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Bacterial and viral pathogens can weaken epithelial barriers by targeting and disrupting tight junction (TJ) proteins. However, comparatively little is known about the direct effects of fungal pathogens on TJ proteins and their expression. The disease chytridiomycosis, caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd), is threatening amphibian populations worldwide. Bd is known to infect amphibian skin and disrupt cutaneous osmoregulation. However, exactly how this occurs is poorly understood. This study considered the impact of Bd infection on the barrier properties of the Australian green tree frog (Litoria caerulea) epidermis by examining how inoculation of animals with Bd influenced the paracellular movement of FITC-dextran (4 kDa, FD-4) across the skin in association with alterations in the mRNA and protein abundance of select TJ proteins of the epidermal TJ complex. It was observed that Bd infection increased paracellular movement of FD-4 across the skin linearly with fungal infection load. In addition, Bd infection increased transcript abundance of the tricellular TJ (tTJ) protein tricellulin (Tric) as well as the bicellular TJ (bTJ) proteins occludin (Ocln), claudin (Cldn)-1, Cldn-4 and the scaffolding TJ protein zonula occludens 1 (ZO-1). However, while Tric protein abundance increased in accord with changes in transcript abundance, protein abundance of Cldn-1 was significantly reduced and Ocln protein abundance was unchanged. Data indicate that disruption of cutaneous osmoregulation in L. caerulea following Bd infection occurs, at least in part, by an increase in epidermal paracellular permeability in association with compromised integrity of the epidermal TJ complex.

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Section: All Examined Tj Protein Transcripts Increase In Abundance Wimentioning

confidence: 99%

A lethal fungal pathogen directly alters tight junction proteins in the skin of a susceptible amphibian

Gauberg

Cramp

et al. 2018

Journal of Experimental Biology

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“…A link between skin barrier function in salt and water balance and the composition and/or abundance of epidermal TJ proteins has been suggested for teleost fishes residing in FW, SW and/or hypersaline SW (Bagherie-Lachidan et al, 2008Bui and Kelly, 2014;Gauberg et al, 2017). Thus, it is likely that increased Ocln abundance in the skin of IPW-acclimated ammocoetes contributed to a decrease in skin permeability.…”

Section: Ammocoete Skinmentioning

confidence: 99%

A role for tight junction-associated MARVEL proteins in larval sea lamprey (Petromyzon marinus) osmoregulation

Kolosov

Bui

Donini

et al. 2017

Journal of Experimental Biology

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This study reports on tight junction-associated MARVEL proteins of larval sea lamprey () and their potential role in ammocoete osmoregulation. Two occludin isoforms (designated Ocln and Ocln-a) and a tricellulin (Tric) were identified. Transcripts encoding , and were broadly expressed in larval lamprey, with the greatest abundance of in the gut, liver and kidney, in the gill and skin, and in the kidney. Ocln and Ocln-a resolved as ∼63 kDa and ∼35 kDa MW proteins, respectively, while Tric resolved as a ∼50 kDa protein. Ocln immunolocalized to the gill vasculature and in gill mucous cells while Ocln-a localized to the gill pouch and gill epithelium. Both Ocln and Ocln-a localized in the nephron, the epidermis and the luminal side of the gut. In branchial tissue, Tric exhibited punctate localization, consistent with its presence at regions of tricellular contact. Following ion-poor water (IPW) acclimation of ammocoetes, serum [Na] and [Cl] decreased, but not [Ca], and carcass moisture content increased. In association, Ocln abundance increased in the skin and kidney, but reduced in the gill of IPW-acclimated ammocoetes while Ocln-a abundance reduced in the kidney only. Tric abundance increased in the gill. Region-specific alterations in , and mRNA abundance were also observed in the gut. Data support a role for Ocln, Ocln-a and Tric in the osmoregulatory strategies of a basal vertebrate.

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“…For example, previous studies have reported both increased and decreased gill cldn-12 mRNA abundance in association with environmental change that requires enhanced barrier function (Chasiotis & Kelly 2011b, Chasiotis et al 2012a, Kolosov et al 2014. Furthermore, cldn-20a has only recently been described in trout as cortisol-responsive in the skin (Gauberg et al 2017), and in this regard, remains to be investigated in the gill. Studies on other vertebrates provide little insight as to the potential compensatory roles of cldn-7, -12 and -20a in the manipulated gill epithelium.…”

Section: The Contribution Of Cldn-8d To Cortisol-mediated Tightening mentioning

confidence: 99%

“…To examine how cldn-8d KD influenced the transcriptional response of other cortisol-responsive cldns, cldn-3a (BK007964), -6 (KF445436), -7 (BK007965), -12 (BK007967), -20a (BK009404), -23a (BK008775), -28b (EU921670), -30 (BK007968) and -31 (BK007969) were chosen for examination in accordance with the observations of Kelly and Chasiotis (2011), Kolosov and coworkers (2014) and Gauberg and coworkers (2017). Transcript abundance of cldns were examined by qPCR using techniques as outlined above, previously published primer sets (Kelly & Chasiotis 2011, Kolosov et al 2014, Gauberg et al 2017 and cDNA were prepared using symmetrically cultured cells.…”

Section: Transcriptional Analysis Of Genes Encoding Cortisolresponsivmentioning

confidence: 99%

Claudin-8d is a cortisol-responsive barrier protein in the gill epithelium of trout

Kolosov

Kelly

2017

Journal of Molecular Endocrinology

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The influence of claudin (Cldn) 8 tight junction (TJ) proteins on cortisol-mediated alterations in gill epithelium permeability was examined using a primary cultured trout gill epithelium model. Genes encoding three Cldn-8 proteins ( and ) have been identified in trout and all are expressed in the model gill epithelium. Cortisol treatment 'tightened' the gill epithelium, as indicated by increased transepithelial resistance (TER) and reduced paracellular [H]polyethylene glycol (MW 400 Da; PEG-400) flux. This occurred in association with elevated mRNA abundance, but no alterations in and mRNA abundance were observed. Transcriptional knockdown (KD) of inhibited a cortisol-induced increase in Cldn-8d abundance and reduced the 'epithelium tightening' effect of cortisol in association with increased paracellular PEG-400 flux. Under simulated conditions (i.e. apical freshwater), KD hindered a cortisol-mediated reduction in basolateral to apical Na and Cl flux (i.e. reduced the ability of cortisol to mitigate ion loss). However, KD did not abolish the tightening effect of cortisol on the gill epithelium. This is likely due, in part, to the effect of cortisol on genes encoding other TJ proteins, which in some cases appeared to exhibit a compensatory response. Data support the idea that Cldn-8d is a barrier protein of the gill epithelium TJ that contributes significantly to corticosteroid-mediated alterations in gill epithelium permeability.

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Claudin tight junction proteins in rainbow trout ( Oncorhynchus mykiss ) skin: Spatial response to elevated cortisol levels

Cited by 11 publications

References 55 publications

A lethal fungal pathogen directly alters tight junction proteins in the skin of a susceptible amphibian

A lethal fungal pathogen directly alters tight junction proteins in the skin of a susceptible amphibian

A role for tight junction-associated MARVEL proteins in larval sea lamprey (Petromyzon marinus) osmoregulation

Claudin-8d is a cortisol-responsive barrier protein in the gill epithelium of trout

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