Further characterization of the sorbitol permease in PAP-HT25 cells

Napathorn, Sophon; Spring, Kenneth R.

doi:10.1152/ajpcell.1994.267.2.c514

Cited by 26 publications

(5 citation statements)

References 9 publications

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“…The size of the substrate is certainly an important factor, with an estimated pore diameter of 0.8‐0.9 nm. However, the rate of polyol permeation is also influenced by the presence and arrangement of hydroxyl groups on the solute, suggesting significant interaction between the channel protein and the permeating solute (Napathorn & Spring, 1994). Similarly, it has been observed that swelling‐activated channels have a higher permeability to β‐amino acids than to similarly sized α‐amino acids (Pasantes‐Morales et al 1994; Roy, 1995).…”

Section: Discussionmentioning

confidence: 99%

Cell volume regulation: the role of taurine loss in maintaining membrane potential and cell pH

Guizouarn

Motais

Garcia-Romeu

et al. 2000

The Journal of Physiology

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In response to a hyposmotic stress cells undergo a regulatory volume decrease (RVD) by losing osmotically active solutes and obliged water. During RVD, trout red cells lost taurine, K+ and Cl− but gained Na+ and Cl−. Over the full time course of RVD the chloride concentration in the cell water remained remarkably constant. Thus membrane potential and cell pH, which depends on the ratio of internal to external chloride concentration ([Cl−]i:[Cl−]o), remained fixed. When cell volume decreases it is only possible to keep the chloride concentration in the cell water constant if an equal percentage of the cell chloride pool and of the cell water pool are lost simultaneously. Quantitative analysis of our data showed that this requirement was fulfilled because, over the full time course of RVD, cells lost osmotically active solutes with a constant stoichiometry: 1 Cl−:1 positive charge:2.35 taurine. Any change in taurine permeability, by modifying the stoichiometric relationship, would affect the amount of water lost and consequently cell chloride concentration. Experiments carried out with different cations as substitutes for external Na+ suggest that the constancy of the chloride concentration is not finely tuned by some mechanism able to modulate the channel transport capacity, but results in part from the fact that the swelling‐dependent channel constitutively possesses an adequately fixed relative permeability for cations and taurine. However, as a significant fraction of K+ and Cl− loss occurs via a KCl cotransporter, the contribution of the cotransport to the stochiometric relationship remains to be defined. The large amount of taurine released during RVD (50 % of all solutes) was shown to be transported as an electroneutral zwitterion and not as an anion. How the channel can accommodate the zwitterionic form of taurine, which possesses a high electrical dipole, is considered.

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Section: Discussionmentioning

confidence: 99%

Cell volume regulation: the role of taurine loss in maintaining membrane potential and cell pH

Guizouarn

Motais

Garcia-Romeu

et al. 2000

The Journal of Physiology

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“…44). With respect to organic solutes, hypotonicity-inducible efflux of sorbitol (18,21,39) and inositol (26,27,33,50,51) has been extensively characterized in cultured cells of the renal medulla and brain, respectively. The signaling events leading to activation of inorganic ion and organic solute efflux pathways remain obscure.…”

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confidence: 99%

Hypotonicity activates transcription through ERK-dependent and -independent pathways in renal cells

Zhang

Yang

Cohen

1998

American Journal of Physiology-Cell Physiology

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Hypotonicity activates transcription through ERK-dependent and -independent pathways in renal cells. Am. J. Physiol. 275 (Cell Physiol. 44): C1104-C1112, 1998.-Acute hypotonic shock (50% dilution of medium with sterile water, but not with isotonic NaCl) activated the extracellular signal response kinase (ERK) mitogen-activated protein (MAP) kinases in renal medullary cells, as measured by Western analysis with a phospho-ERK-specific antibody and by in vitro kinase assay of epitope-tagged ERKs immunoprecipitated from stable HA-ERK transfectants. Hypotonicity also activated the transcription factor and ERK substrate Elk-1 in a partially PD-98059-sensitive fashion, as assessed by chimeric reporter gene assay. Consistent with these data, hypotonic stress activated transcription of the immediate-early gene transcription factor Egr-1 in a partially PD-98059-sensitive fashion. Hypotonicity-inducible Egr-1 transcription was mediated in part through 5Ј-flanking regions containing serum response elements and in part through the minimal Egr-1 promoter. Elimination of the Ets motifs adjacent to key regulatory serum response elements in the Egr-1 promoter diminished the effect of hypotonicity but failed to abolish it. Interestingly, hypotonicity also transiently activated p38 and c-Jun NH 2 -terminal kinase 1, as determined by immunoblotting with anti-phospho-MAP kinase antibodies. Taken together, these data strongly suggest that hypotonicity activates immediate-early gene transcription in renal medullary cells via MAP kinase kinase-dependent and -independent mechanisms. urea; kidney; signal transduction; p38; stress-activated protein kinase; c-Jun amino-terminal kinase ALTHOUGH UBIQUITOUS among prokaryotes and simple eukaryotes, exposure to hypotonicity in higher eukaryotes is generally limited to relatively few epithelia in the absence of systemic disturbances in water balance. In response to water loading or diuresis, cells of the renal medulla encounter a markedly hypotonic milieu (20). In addition, the total solute concentration of a markedly hypertonic renal medullary interstitium, achievable in the face of avid water conservation and comprising a total solute burden Ͼ2,000 mosM, may fall by Ͼ50% in Ͻ1 h after diuresis (5). In response to such physiological anisotonicity, cell volume is acutely regulated through rapid influx or efflux of inorganic ions (e.g., K ϩ and Cl Ϫ ). Thereafter, accumulation or dumping of osmotically active organic solutes called osmolytes ensues (20). In aggregate, these sequential mechanisms achieve the regulatory volume decrease (RVD) essential for maintenance of cell integrity in response to hypotonicity.The molecular mechanisms underlying RVD have received increasing attention; inorganic ion and organic solute efflux pathways have been characterized. Swelling-responsive inorganic ion currents have been observed in diverse systems from prokaryotes to mammalian cells (reviewed in Ref. 8). Among renal epithelia, Cl Ϫ and cation currents have been detected in cells of the proximal tubule (62)...

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“…An inhibition with structural analogs could not be observed [13, 14]. In addition, sorbitol uptake in plasma membrane vesicles from the thick ascending limb of Henle [15]and astrocytes showed no saturation [16].…”

Section: Discussionmentioning

confidence: 99%

“…This cooperation, however, requires a regulated sorbitol release from the basolateral side of IMCD cells and a sorbitol uptake into interstitial cells. The osmotically regulated sorbitol release was extensively investigated by several study groups [3, 6, 13]. However, a sorbitol uptake into renal cells was neither assumed nor examined.…”

Section: Introductionmentioning

confidence: 99%

Evidence for a Sorbitol Transport System in Immortalized Human Renal Interstitial Cells

Grunewald

Ehrhard²,

Fiedler³

et al. 2001

Nephron Exp Nephrol

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Sorbitol plays a major role in the maintenance of cell volume and functional integrity of several renal cells. Sorbitol synthesis takes place in inner collecting duct cells, whereas sorbitol dehydrogenase activity, which catalyzes the degradation of sorbiotol to fructose, could mainly be detected in renal inner medullary interstitial cells. Therefore, we supposed that interstitial cells would require a sorbitol transport into the cells. However, such a transport system has not yet been described. Therefore, we have characterized the uptake of sorbitol in immortalized interstitial TK-173 cells, which were derived from human renal fibroblasts. Comparable to fresh isolated renal fibroblasts of the rat, immortalized TK-173 cells have a high sorbitol dehydrogenase activity. In this report, a temperature-dependent sorbitol uptake with saturation kinetics could be detected in immortalized TK-173 cells. The transport is characterized by a high velocity (V_max 84 mmol/l × h) and an apparent K_m of 10 mmol/l. The sorbitol uptake is independent of membrane potential, sodium, and chloride. Altogether, the physiological characteristics of this sorbitol transport are different from those of the osmotically regulated sorbitol efflux from epithelial cells. These results provide evidence that TK-173 cells derived from renal fibroblasts have a specific sorbitol transport. Furthermore, these data suggest a cooperation between epithelial and interstitial cells concerning osmoregulation.

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Further characterization of the sorbitol permease in PAP-HT25 cells

Cited by 26 publications

References 9 publications

Cell volume regulation: the role of taurine loss in maintaining membrane potential and cell pH

Cell volume regulation: the role of taurine loss in maintaining membrane potential and cell pH

Hypotonicity activates transcription through ERK-dependent and -independent pathways in renal cells

Evidence for a Sorbitol Transport System in Immortalized Human Renal Interstitial Cells

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