Cloning and expression of a cAMP-activated Na+/H+ exchanger: evidence that the cytoplasmic domain mediates hormonal regulation.

Borgèse, Franck; Sardet, Claude; Cappadoro, Marina; Pouysségur, Jacques; Motais, R

doi:10.1073/pnas.89.15.6765

Cited by 136 publications

(77 citation statements)

References 38 publications

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“…Another very strong argument, which points in the direction of two different proteins, is the fact that in trout erythrocytes the (3NHE is quiescent, and becomes only active after stimulation with (3-adrenergic agonists (Motais et al, 1990;Borgese et al, 1992;Guizouam et al, 1993). The Na*/Li* exchange activity, however, is al ways present in the trout erythrocyte.…”

Section: Discussionmentioning

confidence: 99%

“…The second cell line (PS 120) was mutated and did not contain tile Na+/H+ exchanger anymore (L'Allemain et al, 1984). This PS 120 cell line, lacking any Na+/H* exchange activity, was used to overexpress the pNHE (Borgese et al, 1992). This cell line overex pressing the (3NHE was called PS 120-(3NHE.…”

Section: Methodsmentioning

confidence: 99%

“…(A) is the NaVH^ exchanger pNHE, which, as indicated by the equal sign can also exchange Li* for H+. (B) is the protein respon sible for the DMA insensitive Na+/Li+ exchange activity, isopr = isoproterenol, (3 = (3 adrenergic receptor, PKA = protein kinase A, proterenol and inhibited by either DMA or 0 2 (Borggreven et aL, 1995) and therefore can be attributed to the trout erythrocyte Na+/H+ exchanger, ^NHE (Motais, Garcia-Romeu & Borgese, 1987;Motais et ah, 1990;Borgese et al, 1992;Guizouarn et al, 1993). The Na+/ Li+ exchange activity in these membranes, however, was not influenced by either of these components (Borggreven et aL, 1995).…”

Section: Introductionmentioning

confidence: 99%

“…The Li+/H+ activity is normally silent (Mo tais et aL, 1990;Borgese et aL, 1992;Guizouarn et aL, 1993) and can be activated via the P-adrenergic receptor through cAMP. This Li+/H+ activity is DMA and 0 2 sensitive, as can be expected from an exchange activity of the pNHE (Mori et aL, 1991;Borgese et aL, 1992;Guizouarn et aL, 1993). The Na+/Li+ exchange activity, however, is active without stimulation and is not sensi tive to isoproterenol, DMA or 0 2.…”

Section: Introductionmentioning

confidence: 99%

“…To examine whether the DMA-insensitive erythro cyte Na+/Li+ exchange is indeed not a mode of operation of the Na+/H+ exchanger present in these cells, we com pared the exchange activities of human and trout eryth rocytes with those of fibroblast cell lines expressing the Na+/H+ exchangers NHE-1 and (3NHE (L'Allemain, Paris & Pouyssegur, 1984;Pouyssegur et aL, 1984;Borgese et aL, 1992).…”

Section: Introductionmentioning

confidence: 99%

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The Na + /H + Exchanger Present in Trout Erythrocyte Membranes is Not Responsible for the Amiloride-insensitive Na + /Li + Exchange Activity

Norren

Görissen

Borgèse

et al. 1997

Journal of Membrane Biology

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Abstract. The protein responsible for the Na+/Li+ ex change activity across the erythrocyte membrane has not been cloned or isolated. It has been suggested that a Na'TH4' exchanger could be responsible for the Na+/Li+ exchange activity across the erythrocyte membrane. Pre viously, we reported that in the trout erythrocyte, the Li+/H+ exchange activity (mediated by the Na'VH* ex changer 3NHE) and the Na+/Li+ exchange activity re spond differently to cAMP, DMA (dimethyl-amiloride) and 0 2. We concluded that the DMA insensitive Na+/ Li+ exchange activity originates from a different protein.To further examine these findings, we measured Li+ ef flux in fibroblasts expressing the (3NHE as the only Na+/ H+ exchanger. Moreover, the internal pH of these cells was monitored with a fluorescent probe. Our findings indicate that acidification of fibroblasts expressing the Na+/H+ exchanger £NHE, induces a Na+ stimulated Li+ efflux activity in trout erythrocytes. This exchange ac tivity, however, is DMA sensitive and therefore differs from the DMA insensitive Na+/Li+ exchange activity. In these fibroblasts no significant DMA insensitive Na+/ Li* exchange activity was found. These results support the hypothesis that the trout erythrocyte NaVLi* ex change activity is not mediated by the Na+/H+ exchanger (pNHE) present in these membranes.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

The Na + /H + Exchanger Present in Trout Erythrocyte Membranes is Not Responsible for the Amiloride-insensitive Na + /Li + Exchange Activity

Norren

Görissen

Borgèse

et al. 1997

Journal of Membrane Biology

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Mechanisms of acid-base excretion across the gills of a marine fish

et al. 1997

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Na+/H+ and Cl–/HCO3–exchanges in the branchial epithelium are thought to be primarily responsible for acid‐base transfers in fish. Several different cellular mechanisms have been proposed to drive these exchanges in fresh water and marine species. We measured the acid‐base balance and net H+ transfers (ΔH+) in the marine long‐horned sculpin (Myoxocephalus octodecimspinosus) following acidosis. ΔH+ was determined in different groups of acid loaded (2–3 meq kg–1) animals which were: 1) adapted to seawater (SW); 2) adapted to 20% SW; 3) exposed to water with artificially low [Na+] or [Cl–]; 4) exposed to water containing 1 × 10–4 M amiloride, 5‐(N,N‐hexamethylene)‐amiloride (HMA), or 4,4′‐diisothiocyanatostilbene‐2,2′‐disulfonic acid (DIDS). Both seawater and 20% SW adapted fish were able to completely compensate for the infused load and over 24 hours typically over‐excreted more than 2× the amount infused. A 30% decrease in plasma PCO2 following the metabolic acidosis in sculpin adpated to 20% SW (presumably secondary to respiratory alterations) contributed to the rapid recovery of blood pH. Low ambient [Na+] reversed normal acid excretion to an uptake (HCO3– loss; even after acid infusion). 20–30 mM Na+ in the water was necessary to induce a positive ΔH+. A reversible inhibition of ΔH+ was also observed in sculpin exposed to either amiloride or HMA during the acidosis. In contrast, low [Cl–] or DIDS enhanced ΔH+ excretion. We conclude that net H+ excretion measured following acidosis in these seawater or brackish water adapted animals is the sum of parallel (and counter acting) apical gill Na+/H+ and Cl–/HCO3– exchanges. The Na+/H+ transfers are most likely via an antiporter of the NHE family and occur on the background of continued “band‐3” Cl–/HCO3– exchange. J. Exp. Zool. 279:509–520, 1997.© 1997 Wiley‐Liss, Inc.

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