Regulation of intracellular pH in cultured bovine retinal pigment epithelial cells

Keller, Svea K.; Jentsch, Thomas J.; Janicke, Ilse; Wiederholt, Michael

doi:10.1007/bf00581645

Cited by 27 publications

(18 citation statements)

References 30 publications

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“…The co-existence of these two exchangers has been described previously in diverse mammalian preparations (Kimelberg et al 1979;Chaillet et al 1986;Kurtz & Golchini, 1987;Paradiso, Tsien, Demarest & Machen, 1987;Keller, Jentsch, Janicke & Wiederholt, 1988;Korbmacher, Helbig, Stahl & Wiederholt, 1988;Nord, Brown & Crandall, 1988;Redhead, 1988;Vigne et al 1988). …”

Section: Mechanism Of Acid Extrusion In Purkinje Cellsmentioning

confidence: 95%

Ionic control of intracellular pH in rat cerebellar Purkinje cells maintained in culture.

Gaillard

Dupont

1990

The Journal of Physiology

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SUMMARY1. Intracellular pH (pHi) was measured in single rat cerebellar Purkinje cells maintained in primary culture using microspectrofluorescence analysis of the intracellularly trapped pH-sensitive dye 2',7'-bis-(2-carboxyethyl)-5 (and -6)-carboxyfluorescein (BCECF).2. The ratio of the fluorescence signals measured at 530 nm in response to an alternating excitation at 450 and 490 nm was calibrated using the K+-H+ ionophore nigericin. This calibration gave a steady-state pHi of 7-06 + 0-02 (S.E.M., n = 17) when cells were perfused by a 5 % C02-25 mM-HCO3--buffered solution at an external pH of 7 40 at 37 0C.3. Replacement of external chloride with gluconate in the presence of bicarbonate induced a cytoplasmic alkalinization of about 0 3 pH unit. This alkalinization was independent of external sodium and was greatly reduced by 0 5 mM-DIDS, indicating the presence of a chloride-bicarbonate exchange.4. In bicarbonate-free (HEPES-buffered) solution the steady-state pHi was 7-37 +002 (n = 19), significantly higher than in bicarbonate-buffered solution. Recovery from an intracellular acid load brought about by the ammonium chloride pre-pulse technique was blocked by the removal of external sodium or the addition of 1-5 mM-amiloride, indicating the presence of a sodium-hydrogen exchange.5. In bicarbonate-buffered solution pHi recovery after an acid load was also completely blocked by addition of 1-5 mM-amiloride indicating the absence of a bicarbonate-dependent acid extrusion mechanism.6. Addition of 12-O-tetradecanoylphorbol-13-acetate (TPA, 100 nM) induced an amiloride-sensitive alkalinization of about 0 3 pH unit in bicarbonate-buffered solution but had no effect in HEPES-buffered solution. This observation suggests that in cultured Purkinje cells the sodium-hydrogen exchanger could be activated through a protein kinase C pathway only when pHi is maintained at a low physiological value by the activity of the chloride-bicarbonate exchange.

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Section: Mechanism Of Acid Extrusion In Purkinje Cellsmentioning

confidence: 95%

Ionic control of intracellular pH in rat cerebellar Purkinje cells maintained in culture.

Gaillard

Dupont

1990

The Journal of Physiology

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“…An electroneutral, amiloride-sensitive Na+-H+ exchanger has recently been described in cultured bovine retinal pigment epithelial cells (Keller et al 1988). In the retinal membrane of the frog retinal pigment epithelium, such a transport system can only be of little significance since no intracellular acidification was observed when Na+ was removed in the absence of HC03-and since 1 mM-amiloride had no effects on the rates of change in the intracellular parameters in the transient experiments.…”

Section: Effects Of Changes In the Hc03-concentrationmentioning

confidence: 99%

Rheogenic sodium‐bicarbonate co‐transport across the retinal membrane of the frog retinal pigment epithelium.

Cour

1989

The Journal of Physiology

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SUMMARY1. Na+ and HC03-transport across the retinal membrane of the frog retinal pigment epithelium was studied by means of double-barrelled Na+-and pH-selective microelectrodes. Transient changes in the intracellular pH and in the intracellular Na+ activity were monitored in response to abrupt changes in the Na+ concentration and in the HC03-concentration on the retinal side of the epithelium, and in response to transepithelial currents.2. Removal of Na+ from the retinal side of the epithelium caused a depolarization of the membrane potential across the retinal membrane, a decrease in the intracellular Na+ activity and a decrease in the intracellular pH.3. An increase in the HC03-concentration on the retinal side of the epithelium from 27-5 to 50 mm caused a hyperpolarization of the membrane potential across the retinal membrane, an increase in the intracellular Na+ activity and an increase in the intracellular pH.4. Passage of a transepithelial current of 30 ,uA in the choroid-to-retina direction caused an increase in the intracellular Na+ activity and an increase in the intracellular pH.

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“…For these functions, a large number of pathways which enable the flux of ions across the cell membrane are present in RPE cells. These pathways include ion transporter systems such as the Na + /K + -ATPase [located in the apical membrane, Rizzolo and Zhou, 1995], the Na + /Ca 2+ exchanger [Fijisawa et al, 1993], the Na + /H + exchanger [Keller et al, 1988] cotransporter [LaCour, 1989;LaCour, 1991] and the HCO 3 -/ Cl -exchanger [Keller et al, 1988]. In addition, freshly isolated and cultured cells express ion channels for potassium [Hughes and Steinberg, 1990;Fox and Steinberg, 1992;Wen et al, 1993;Segawa and Hughes, 1994;Strauss et al, 1994;Tao et al, 1994;Tao and Kelly, 1995;Hughes and Takahira, 1996], calcium [Ueda and Steinberg, 1993;Strauss and Wienrich, 1994a, b], sodium [Botchkin and Matthews, 1994;Wen et al, 1994] and chloride [Botchkin and Matthews, 1993;Hughes and Segawa, 1993;Ueda and Steinberg, 1994;Strauss et al, 1996Strauss et al, , 1997 as well as nonselective cation channels [Fox et al, 1988;Poyer et al, 1996].…”

Section: Function Of the Normal Rpementioning

confidence: 99%

The Royal College of Surgeons Rat: An Animal Model for Inherited Retinal Degeneration with a Still Unknown Genetic Defect

Strauß

Stumpff²,

Mergler³

et al. 1998

Cells Tissues Organs

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The Royal College of Surgeons (RCS) rat is the first known animal with inherited retinal degeneration. Despite the fact that the genetic defect is not known, the RCS rat is widely used for research in hereditary retinal dystrophies. This review tries to summarize observations which have been made in the RCS rat and to make an attempt to formulate candidate genes which may the cause for the retinal degeneration in this rat strain. The genetic defect in RCS rats causes the inability of the retinal pigment epithelium (RPE) to phagocytose shed photoreceptor outer segments. In normal rats or humans, this circadian process is regulated by both the cyclic adenosine monophosphate (cAMP) and the calcium/ inositol phosphate systems. The calcium/inositol phosphate system seems to be linked to the phagocytosis receptors which recognize photoreceptor outer membranes to initialize phagocytosis. The cAMP system appeared as modulator of the regulation of phagocytosis. An increase in the intracellular cAMP concentration is an ‘off’ signal for phagocytosis. In RPE cells from RCS rats many observations have been made which indicate a changed second messenger metabolism concerning both the cAMP and the calcium/inositol phosphate systems. The genetic defect seems to concern a protein which is involved in the initialization of a second messenger pathway. We conclude that the genes coding for the phagocytosis receptor or for proteins which are linked to receptors (for example G proteins) are good candidates for defective genes in RCS rats.

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Regulation of intracellular pH in cultured bovine retinal pigment epithelial cells

Cited by 27 publications

References 30 publications

Ionic control of intracellular pH in rat cerebellar Purkinje cells maintained in culture.

Ionic control of intracellular pH in rat cerebellar Purkinje cells maintained in culture.

Rheogenic sodium‐bicarbonate co‐transport across the retinal membrane of the frog retinal pigment epithelium.

The Royal College of Surgeons Rat: An Animal Model for Inherited Retinal Degeneration with a Still Unknown Genetic Defect

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