Regulatory volume response following hypotonic stress in Atlantic salmon erythrocytes

Wormser, Chloe; Mason, L; Helm, Ethan; Light, Douglas B.

doi:10.1007/s10695-011-9474-3

Cited by 8 publications

(6 citation statements)

References 43 publications

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“…Changes in macromolecular density are intimately linked to cell volume changes. Experiments with primary fish cells isolated from a wide variety of tissues have shown an abundance of molecular responses to osmotically induced changes in cell volume, and the corresponding literature is too extensive to be reviewed here (6,16,40,73,88,107,108,178,193). Some of these studies imply that membrane stretch is a trigger for osmosensory signal transduction.…”

Section: The Role Of Macromolecular Crowding and Damage For Osmosensingmentioning

confidence: 99%

The Combinatorial Nature of Osmosensing in Fishes

Kültz

2012

Physiology

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Organisms exposed to altered salinity must be able to perceive osmolality change because metabolism has evolved to function optimally at specific intracellular ionic strength and composition. Such osmosensing comprises a complex physiological process involving many elements at organismal and cellular levels of organization. Input from numerous osmosensors is integrated to encode magnitude, direction, and ionic basis of osmolality change. This combinatorial nature of osmosensing is discussed with emphasis on fishes.

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Section: The Role Of Macromolecular Crowding and Damage For Osmosensingmentioning

confidence: 99%

The Combinatorial Nature of Osmosensing in Fishes

Kültz

2012

Physiology

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“…This homeostatic response has been mostly investigated in mammalian cells but also in cells of lower vertebrates and invertebrates. Cell volume regulation has been observed in numerous cell types, such as astrocytes [5], erythrocytes from different sources [6,7], lymphocytes [8] and sperm [9]. RVD was also studied in invertebrate cells [10][11][12][13][14][15][16], although details of its mechanisms are still missing.…”

Section: Introductionmentioning

confidence: 99%

Evidence for Aquaporin-mediated Water Transport in Nematocytes of the Jellyfish <i>Pelagia noctiluca</i>

Marino

Morabito

Spada

et al. 2011

Cell Physiol Biochem

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Nematocytes, the stinging cells of Cnidarians, have a cytoplasm confined to a thin rim. The main cell body is occupied by an organoid, the nematocyst, containing the stinging tubule and venom. Exposed to hypotonic shock, nematocytes initially swell during an osmotic phase (OP) and then undergo regulatory volume decrease (RVD) driven by K⁺, Cl^- and obligatory water extrusion mechanisms. The purpose of this report is to characterize the OP. Nematocytes were isolated by the NaSCN/Ca²⁺ method from tentacles of the jellyfish Pelagia noctiluca, collected in the Strait of Messina, Italy. Isolated nematocytes were subjected to hyposmotic shock in 65% artificial seawater (ASW) for 15 min. The selective aquaporin water channel inhibitor HgCl₂ (0.1-25 µM) applied prior to osmotic shock prevented the OP and thus RVD. These effects were attenuated in the presence of 1mM dithiothreitol (DTT), a mercaptide bond reducing agent. AgNO₃ (1 µM) and TEA (tetraethylammonium, 100 µM), also reported to inhibit water transport, did not alter the OP but significantly diminished RVD, suggesting different modes of action for the inhibitors tested. Based on estimates of the nematocyte surface area and volume, and OP duration, a relative water permeability of ∼10^-7 cm/sec was calculated and the number of putative aquaporin molecules mediating the OP was estimated. This water permeability is 3-4 orders of magnitude lower in comparison to higher order animals and may constitute an evolutionary advantage for Cnidarian survival.

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“…Besides, the sources of [Ca 2+ ] i transients observed during the RVD and the RVI processes are different and the possible link between [Ca 2+ ] i increase and the RVI process has not been elucidated (Marino & La Spada, ; Wormser et al . ). Some studies have indicated that the [Ca 2+ ] i increase in response to hyperosmolarity is due to NKCC1 activity, which allows membrane depolarization (van Mil et al .…”

Section: Discussionmentioning

confidence: 97%

Osmosensation in TRPV2 dominant negative expressing skeletal muscle fibres

Zanou

Mondin

Fuster

et al. 2015

The Journal of Physiology

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Key pointsr Increased plasma osmolarity induces intracellular water depletion and cell shrinkage (CS) followed by activation of a regulatory volume increase (RVI).r In skeletal muscle, the hyperosmotic shock-induced CS is accompanied by a small membrane depolarization responsible for a release of Ca 2+ from intracellular pools.r Hyperosmotic shock also induces phosphorylation of STE20/SPS1-related proline/alanine-rich kinase (SPAK).r TRPV2 dominant negative expressing fibres challenged with hyperosmotic shock present a slower membrane depolarization, a diminished Ca 2+ response, a smaller RVI response, a decrease in SPAK phosphorylation and defective muscle function.r We suggest that hyperosmotic shock induces TRPV2 activation, which accelerates muscle cell depolarization and allows the subsequent Ca 2+ release from the sarcoplasmic reticulum, activation of the Na + -K + -Cl − cotransporter by SPAK, and the RVI response.Abstract Increased plasma osmolarity induces intracellular water depletion and cell shrinkage followed by activation of a regulatory volume increase (RVI). In skeletal muscle, this is accompanied by transverse tubule (TT) dilatation and by a membrane depolarization responsible for a release of Ca 2+ from intracellular pools. We observed that both hyperosmotic shock-induced Ca 2+ transients and RVI were inhibited by Gd 3+ , ruthenium red and GsMTx4 toxin, three inhibitors of mechanosensitive ion channels. The response was also completely absent in muscle fibres overexpressing a non-permeant, dominant negative (DN) mutant of the transient receptor potential, V2 isoform (TRPV2) ion channel, suggesting the involvement of TRPV2 or of a TRP isoform susceptible to heterotetramerization with TRPV2. The release of Ca 2+ induced by hyperosmotic shock was increased by cannabidiol, an activator of TRPV2, and decreased by tranilast, an inhibitor of TRPV2, suggesting a role for the TRPV2 channel itself. Hyperosmotic shock-induced membrane depolarization was impaired in TRPV2-DN fibres, suggesting that TRPV2 activation triggers the release of Ca 2+ from the sarcoplasmic reticulum by depolarizing TTs. RVI requires the sequential activation of STE20/SPS1-related proline/alanine-rich kinase (SPAK) and NKCC1, a Na + -K + -Cl − cotransporter, allowing ion entry and driving osmotic water flow. In fibres overexpressing TRPV2-DN as well as in fibres in which Ca 2+ transients were abolished by the Ca 2+ chelator BAPTA, the level of P-SPAK Ser373 in response to hyperosmotic shock was reduced, suggesting a modulation of SPAK phosphorylation by intracellular Ca 2+ . We conclude that TRPV2N. Zanou and L. Mondin contributed equally to this work. is involved in osmosensation in skeletal muscle fibres, acting in concert with P-SPAK-activated NKCC1.( -96365, 1-[β-[3-(4-methoxyphenyl) propoxy]-4-methoxyphenetyl]-1H-imidazole); SPAK, STE20/SPS1-related proline/alanine-rich kinase; TRPV2, transient receptor potential, V2 isoform; TRPV2-DN, dominant negative mutant of TRPV2; TT, transverse tubule; WNK protein kinase, with-no-...

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Regulatory volume response following hypotonic stress in Atlantic salmon erythrocytes

Cited by 8 publications

References 43 publications

The Combinatorial Nature of Osmosensing in Fishes

The Combinatorial Nature of Osmosensing in Fishes

Evidence for Aquaporin-mediated Water Transport in Nematocytes of the Jellyfish <i>Pelagia noctiluca</i>

Osmosensation in TRPV2 dominant negative expressing skeletal muscle fibres

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