Production of eicosanoids by the killifish gills and opercular epithelia and their effect on active transport of ions

Praag, Dina Van; Farber, Saul J.; Minkin, Eric; Primor, Naftali

doi:10.1016/0016-6480(87)90204-8

Cited by 56 publications

(29 citation statements)

References 17 publications

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“…Two early studies demonstrated that PGE 2 inhibited the I sc across the killifish opercular epithelium (171,770), and a recent study found that PGE 2 inhibited the I sc produced by a cultured epithelium of PVCs from the sea bass (Dicentrarchus labrax; Ref. 15).…”

Section: Prostanoidsmentioning

confidence: 99%

The Multifunctional Fish Gill: Dominant Site of Gas Exchange, Osmoregulation, Acid-Base Regulation, and Excretion of Nitrogenous Waste

Evans¹,

Piermarini²,

Choe³

2005

Physiological Reviews

2,320

1,788

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The fish gill is a multipurpose organ that, in addition to providing for aquatic gas exchange, plays dominant roles in osmotic and ionic regulation, acid-base regulation, and excretion of nitrogenous wastes. Thus, despite the fact that all fish groups have functional kidneys, the gill epithelium is the site of many processes that are mediated by renal epithelia in terrestrial vertebrates. Indeed, many of the pathways that mediate these processes in mammalian renal epithelial are expressed in the gill, and many of the extrinsic and intrinsic modulators of these processes are also found in fish endocrine tissues and the gill itself. The basic patterns of gill physiology were outlined over a half century ago, but modern immunological and molecular techniques are bringing new insights into this complicated system. Nevertheless, substantial questions about the evolution of these mechanisms and control remain.

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Section: Prostanoidsmentioning

confidence: 99%

The Multifunctional Fish Gill: Dominant Site of Gas Exchange, Osmoregulation, Acid-Base Regulation, and Excretion of Nitrogenous Waste

Evans¹,

Piermarini²,

Choe³

2005

Physiological Reviews

2,320

1,788

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“…This tissue is the primary site of osmoregulation in fishes and contains specialized cells that secrete NaCl (chloride cells) via a mechanism that is similar to the NaCl transport mechanism of shark rectal glands and the mammalian cortical thick ascending limb of the kidney . Using isolated opercular epithelia of killifish (Fundulus heteroclitus), a well-established model for the gill epithelium that can be mounted in modified Ussing chambers (Karnaky, Jr et al, 1977;Eriksson et al, 1985), we and others have demonstrated that prostaglandins inhibit short circuit currents (I sc ) that are a result of active Cl -secretion (Van Praag et al, 1987;. Using specific pharmacological inhibitors, we also determined that basal I sc may be moderately inhibited by COX2-mediated prostaglandin synthesis and that COX2 mediated a large fraction of endothelin-induced inhibition of I sc .…”

Section: Introductionmentioning

confidence: 99%

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

Choe

Havird

Rose

et al. 2006

Journal of Experimental Biology

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SUMMARY In the kidneys of mammals, cyclooxygenase type 2 (COX2) is expressed in medullary interstitial cells, the macula densa and epithelial cells of the cortical thick ascending limb where it generates prostaglandins that regulate hormone secretion, inhibit ion transport, and support cell survival during salt loading and dehydration. In teleosts, the gills are in direct contact with an aquatic environment and are the dominant site of osmoregulation. During transfers between salinities, specialized cells in the gills (chloride cells) rapidly regulate NaCl secretion for systemic osmoregulation while they simultaneously are exposed to acute osmotic shock. This study was conducted to determine if COX2 is expressed in the gills, and if so, to evaluate its function in cellular and systemic osmoregulation. Degenerate primers, reverse transcription–PCR and rapid amplification of cDNA ends were used to deduce the complete cDNA sequence of a putative COX2 enzyme from the gills of the euryhaline killifish (Fundulus heteroclitus). The 2738 base pair cDNA includes a coding region for a 610 amino acid protein that is over 70%identical to mammalian COX2. A purified antibody generated against a conserved region of mouse COX2 labeled chloride cells, suggesting that the enzyme may control NaCl secretion as an autocrine agent. Real-time PCR was then used to demonstrate that mRNA expression of the COX2 homologue was threefold greater in gills from chronic seawater killifish than in gills from chronic freshwater killifish. Expression of Na+/K+/2Cl–cotransporter and the cystic fibrosis transmembrane conductance regulator were also greater in seawater, suggesting that chronic COX2 expression in the gills is regulated in parallel to the key ion transporters that mediate NaCl secretion. Real-time PCR was also used to demonstrate that acute transfer from seawater to freshwater and from freshwater to seawater led to rapid, transient inductions of COX2 expression. Together with previous physiological evidence,the present molecular and immunological data suggest that constitutive branchial COX2 expression is enhanced in seawater, where prostaglandins can regulate NaCl secretion in chloride cells. Our data also suggest that branchial COX2 expression may play a role in cell survival during acute osmotic shock.

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“…In the vertebrate cell line Ehrlich ascites tumour cells, it has been demonstrated that cytoplasmic phospholipase A 2 (cPLA 2 ) is activated by hypotonic shock, resulting in increase of arachidonic acid release and increased eicosanoid synthesis (Hoffmann, 2000). The eicosanoid prostaglandin E 2 (PGE 2 ) is known to rapidly inhibit Cl -secretion in the opercular membrane of Fundulus heteroclitus (Eriksson et al, 1985;Van Praag et al, 1987;Evans et al, 2003) and the tissue metabolizes several different eicosanoids, including prostaglandins, leukotrienes and hydroxyeicosatetraenoic acids (Van Praag et al, 1987). While thromboxanes and carbaprostacyclin (a PGI2 analogue) do not affect ion secretion rate, there appear to be both inhibitory and stimulatory PGE2 receptors in the killifish opercular epithelium (Evans et al, 2004).…”

mentioning

confidence: 99%

Hypotonic shock mediation by p38 MAPK, JNK, PKC, FAK, OSR1 and SPAK in osmosensing chloride secreting cells of killifish opercular epithelium

Marshall

Ossum

Hoffmann

2005

Journal of Experimental Biology

110

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SUMMARY Hypotonic shock rapidly inhibits Cl- secretion by chloride cells, an effect that is osmotic and not produced by NaCl-depleted isosmotic solutions, yet the mechanism for the inhibition and its recovery are not known. We exposed isolated opercular epithelia, mounted in Ussing chambers, to hypotonic shock in the presence of a variety of chemicals: a general protein kinase C (PKC) inhibitor chelerythrine, Gö6976 that selectively blocks PKCα and β subtypes, H-89 that blocks PKA, SB203580 that blocks p38 mitogen-activated protein kinase (MAPK), as well as serine/threonine protein phosphatase (PP1 and 2A) inhibitor okadaic acid, and finally tamoxifen, a blocker of volume-activated anion channels (VSOAC). Chelerythrine has no effect on hypotonic inhibition but blocked the recovery, indicating PKC involvement in stimulation. Gö6976 had little effect, suggesting that PKCα and PKCβ subtypes are not involved. H-89 did not block hypotonic inhibition but decreased the recovery, indicating PKA may be involved in the recovery and overshoot (after restoration of isotonic conditions). SB203580 significantly enhanced the decrease in current by hypotonic shock, suggesting an inhibitory role of p38 MAPK in the hypotonic inhibition. Okadaic acid increased the steady state current, slowed the hypotonic inhibition but made the decrease in current larger; also the recovery and overshoot were completely blocked. Hypotonic stress rapidly and transiently increased phosphorylated p38 MAPK (pp38) MAPK (measured by western analysis) by eightfold at 5 min, then more slowly again to sevenfold at 60 min. Hypertonic shock slowly increased p38 by sevenfold at 60 min. Phosphorylated JNK kinase was increased by 40-50% by both hypotonic and hypertonic shock and was still elevated at 30 min in hypertonic medium. By immunoblot analysis it was found that the stress protein kinase (SPAK) and oxidation stress response kinase 1 (OSR1) were present in salt and freshwater acclimated fish with higher expression in freshwater. By immunocytochemistry,SPAK, OSR1 and phosphorylated focal adhesion kinase (pFAK) were colocalized with NKCC at the basolateral membrane. The protein tyrosine kinase inhibitor genistein (100 μmol l-1) inhibited Cl- secretion that was high, increased Cl- secretion that was low and reduced immunocytochemical staining for phosphorylated FAK. We present a model for rapid control of CFTR and NKCC in chloride cells that includes: (1) activation of NKCC and CFTR via cAMP/PKA, (2) activation of NKCC by PKC, myosin light chain kinase (MLCK), p38, OSR1 and SPAK, (3) deactivation of NKCC by hypotonic cell swelling, Ca2+ and an as yet unidentified protein phosphatase and (4) involvement of protein tyrosine kinase (PTK) acting on FAK to set levels of NKCC activity.

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Production of eicosanoids by the killifish gills and opercular epithelia and their effect on active transport of ions

Cited by 56 publications

References 17 publications

The Multifunctional Fish Gill: Dominant Site of Gas Exchange, Osmoregulation, Acid-Base Regulation, and Excretion of Nitrogenous Waste

The Multifunctional Fish Gill: Dominant Site of Gas Exchange, Osmoregulation, Acid-Base Regulation, and Excretion of Nitrogenous Waste

COX2 in a euryhaline teleost,Fundulus heteroclitus: primary sequence, distribution, localization, and potential function in gills during salinity acclimation

Hypotonic shock mediation by p38 MAPK, JNK, PKC, FAK, OSR1 and SPAK in osmosensing chloride secreting cells of killifish opercular epithelium

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