Novel discoveries in acid-base regulation and osmoregulation: A review of selected hormonal actions in zebrafish and medaka

Yan, Jia‐Jiun; Hwang, Pung‐Pung

doi:10.1016/j.ygcen.2019.03.007

Cited by 47 publications

(47 citation statements)

References 121 publications

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“…Krüppel-like factor 4 (Klf4) plays an important role in maintaining the ionocyte progenitor cell pool by stimulating epidermal cell stem proliferation (Chen et al, 2019). In addition, several hormones, including isotocin, cortisol and stanniocalcin 1, have been implicated in the regulation of the ionocyte progenitor cell pool (Chou et al, 2011; Chou et al, 2015; Yan and Hwang, 2019). Foxi3a/3b form a positive regulatory loop and this loop is critical in specifying ionocyte progenitors to give rise to the 5 types of ionocytes (Chang et al, 2009; Hsiao et al, 2007; Yan and Hwang, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, several hormones, including isotocin, cortisol and stanniocalcin 1, have been implicated in the regulation of the ionocyte progenitor cell pool (Chou et al, 2011; Chou et al, 2015; Yan and Hwang, 2019). Foxi3a/3b form a positive regulatory loop and this loop is critical in specifying ionocyte progenitors to give rise to the 5 types of ionocytes (Chang et al, 2009; Hsiao et al, 2007; Yan and Hwang, 2019). A hallmark of NaR cells is the expression of Trpv6 (Liu et al, 2017; Pan et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…In zebrafish, trpv6 is specifically expressed in a population of epithelial cells known as ionocytes or NaR cells (Dai et al, 2014; Pan et al, 2005). NaR cells take up Ca 2+ from the surrounding habitats into the body to maintain body Ca 2+ homeostasis (Liao et al, 2009; Yan and Hwang, 2019). NaR cells are polarized cells that functionally and molecularly similar to human intestinal epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

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Cell-autonomous regulation of epithelial cell quiescence by calcium channel Trpv6

Malick

et al. 2019

eLife

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Epithelial homeostasis and regeneration require a pool of quiescent cells. How the quiescent cells are established and maintained is poorly understood. Here, we report that Trpv6, a cation channel responsible for epithelial Ca2+ absorption, functions as a key regulator of cellular quiescence. Genetic deletion and pharmacological blockade of Trpv6 promoted zebrafish epithelial cells to exit from quiescence and re-enter the cell cycle. Reintroducing Trpv6, but not its channel dead mutant, restored the quiescent state. Ca2+ imaging showed that Trpv6 is constitutively open in vivo. Mechanistically, Trpv6-mediated Ca2+ influx maintained the quiescent state by suppressing insulin-like growth factor (IGF)-mediated Akt-Tor and Erk signaling. In zebrafish epithelia and human colon carcinoma cells, Trpv6/TRPV6 elevated intracellular Ca2+ levels and activated PP2A, which down-regulated IGF signaling and promoted the quiescent state. Our findings suggest that Trpv6 mediates constitutive Ca2+ influx into epithelial cells to continuously suppress growth factor signaling and maintain the quiescent state.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cell-autonomous regulation of epithelial cell quiescence by calcium channel Trpv6

Malick

et al. 2019

eLife

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“…As a consequence, it can be hypothesized that diverse isoforms of glutamate/glutamine-regulating enzymes exhibit different functions in teleost epithelium, and these isoforms differentially respond to hyperosmotic changes. Here it should be noted that despite the very similar overall function and cellular equipment of gill epithelia and the yolk integument [60][61][62][63] we cannot rule out the possibility that there are some differences in gene expression patterns between larval and adult branchial epithelia.…”

Section: Glutamate and Glutamine Metabolism In Gills Of Euryhaline Tementioning

confidence: 86%

Energy and nitrogenous waste from glutamate/glutamine catabolism facilitates acute osmotic adjustment in non-neuroectodermal branchial cells

Huang

Liu

et al. 2020

Sci Rep

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Maintenance of homeostasis is one of the most important physiological responses for animals upon osmotic perturbations. Ionocytes of branchial epithelia are the major cell types responsible for active ion transport, which is mediated by energy-consuming ion pumps (e.g., Na+-K+-ATPase, NKA) and secondary active transporters. Consequently, in addition to osmolyte adjustments, sufficient and immediate energy replenishment is essenttableial for acclimation to osmotic changes. In this study, we propose that glutamate/glutamine catabolism and trans-epithelial transport of nitrogenous waste may aid euryhaline teleosts Japanese medaka (Oryzias latipes) during acclimation to osmotic changes. Glutamate family amino acid contents in gills were increased by hyperosmotic challenge along an acclimation period of 72 hours. This change in amino acids was accompanied by a stimulation of putative glutamate/glutamine transporters (Eaats, Sat) and synthesis enzymes (Gls, Glul) that participate in regulating glutamate/glutamine cycling in branchial epithelia during acclimation to hyperosmotic conditions. In situ hybridization of glutaminase and glutamine synthetase in combination with immunocytochemistry demonstrate a partial colocalization of olgls1a and olgls2 but not olglul with Na+/K+-ATPase-rich ionocytes. Also for the glutamate and glutamine transporters colocalization with ionocytes was found for oleaat1, oleaat3, and olslc38a4, but not oleaat2. Morpholino knock-down of Sat decreased Na+ flux from the larval epithelium, demonstrating the importance of glutamate/glutamine transport in osmotic regulation. In addition to its role as an energy substrate, glutamate deamination produces NH4+, which may contribute to osmolyte production; genes encoding components of the urea production cycle, including carbamoyl phosphate synthetase (CPS) and ornithine transcarbamylase (OTC), were upregulated under hyperosmotic challenges. Based on these findings the present work demonstrates that the glutamate/glutamine cycle and subsequent transepithelial transport of nitrogenous waste in branchial epithelia represents an essential component for the maintenance of ionic homeostasis under a hyperosmotic challenge.

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“…Our recent studies using a zebrafish model suggested a similar role of IGF-PI3 kinase-Akt-Tor signaling in regulating the proliferation-quiescence balance in a population of epithelial cells (Dai et al, 2014;Liu et al, 2017). These mitochondria-rich cells, known as ionocytes or NaR cells, take up Ca 2+ from the surrounding aquatic habitat to maintain body Ca 2+ homeostasis (Hwang, 2009;Yan and Hwang, 2019). In the adult stage, NaR cells are distributed in the adult gills, intestine, and kidney, key organs for Ca 2+ uptake and reabsorption.…”

Section: Introductionmentioning

confidence: 99%

Stanniocalcin 1a is a Ca²⁺-regulated switch controlling epithelial cell quiescence-proliferation balance and Ca²⁺uptake

Liu

Goldstein

et al. 2020

Preprint

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The mechanisms governing cell quiescence-proliferation balance are poorly defined. Using a zebrafish model, here we report that Stc1a, a glycoprotein known as a hypocalcemic hormone, not only inhibits epithelial calcium uptake but also functions as a Ca2+-regulated switch controlling epithelial cell quiescence-proliferation balance. Among the 4 stc genes, only the stc1a expression is [Ca2+]-dependent. Genetic deletion of stc1a, but not stc2b, resulted in elevated body Ca2+ contents, ectopic Ca2+ deposit, body swelling, and premature death. Reducing epithelial calcium channel Trpv6-mediated Ca2+ uptake alleviated these phenotypes. Loss of Stc1a also promoted quiescent epithelial cells to re-enter the cell cycle. This action was accompanied by local IGF signaling activation and increased expression in papp-aa, a zinc metalloproteinase degrading Igfbp5a. Genetic deletion of papp-aa or igfbp5a abolished the elevated epithelial cell reactivation in stc1a−/− mutants. Likewise, inhibition of IGF1 receptor, PI3 kinase, Akt, and Tor signaling abolished epithelial cell reactivation. These results reveal that Stc1a plays dual roles in regulating epithelial calcium uptake and cell quiescence-proliferation balance and implicate Trpv6 and Papp-aa-Igfbp5a-IGF signaling in these functions.

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Novel discoveries in acid-base regulation and osmoregulation: A review of selected hormonal actions in zebrafish and medaka

Cited by 47 publications

References 121 publications

Cell-autonomous regulation of epithelial cell quiescence by calcium channel Trpv6

Cell-autonomous regulation of epithelial cell quiescence by calcium channel Trpv6

Energy and nitrogenous waste from glutamate/glutamine catabolism facilitates acute osmotic adjustment in non-neuroectodermal branchial cells

Stanniocalcin 1a is a Ca²⁺-regulated switch controlling epithelial cell quiescence-proliferation balance and Ca²⁺uptake

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Novel discoveries in acid-base regulation and osmoregulation: A review of selected hormonal actions in zebrafish and medaka

Cited by 47 publications

References 121 publications

Cell-autonomous regulation of epithelial cell quiescence by calcium channel Trpv6

Cell-autonomous regulation of epithelial cell quiescence by calcium channel Trpv6

Energy and nitrogenous waste from glutamate/glutamine catabolism facilitates acute osmotic adjustment in non-neuroectodermal branchial cells

Stanniocalcin 1a is a Ca2+-regulated switch controlling epithelial cell quiescence-proliferation balance and Ca2+uptake

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Stanniocalcin 1a is a Ca²⁺-regulated switch controlling epithelial cell quiescence-proliferation balance and Ca²⁺uptake