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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      The Opossum Kidney Cell Type IIa Na/P i Cotransporter Is a Phosphoprotein

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          Abstract

          Background/Aim: Parathyroid hormone (PTH)-dependent inhibition of proximal tubular P<sub>i</sub> reabsorption is mediated by protein kinase A and/or C and is associated with reduced border membrane expression of the type IIa Na/P<sub>i</sub> cotransporter. The aim of this study was to analyze phosphorylation of the type IIa cotransporter protein. Methods: Opossum kidney cells were used as a ‘proximal tubular’ cell model. Protein phosphorylation was determined by immunoprecipitation of the type IIa Na/P<sub>i</sub> cotransporter, followed by autoradiography. The transporter protein content was evaluated by Western blotting and transport activity by tracer P<sub>i</sub> uptake. Results: Under control conditions (no PTH) the transporter was phosphorylated; upon treatment with PTH, a decrease in phosphorylation was observed. A protein phosphatase inhibitor (okadaic acid) was unable to prevent PTH-induced Na/P<sub>i</sub> cotransporter inhibition but reduced transporter degradation. Conclusion: The type IIa Na/P<sub>i</sub> cotransporter is a phosphoprotein, but alterations in its phosphorylation seem not to be involved in P<sub>i</sub> transport inhibition.

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          Parathyroid hormone leads to the lysosomal degradation of the renal type II Na/Pi cotransporter.

          I Ruf, Heini Murer, Susan Lederer … (1998)
          We have studied the involvement of proteolytic pathways in the regulation of the Na/Pi cotransporter type II by parathyroid hormone (PTH) in opossum kidney cells. Inhibition of lysosomal degradation (by leupeptin, ammonium chloride, methylamine, chloroquine, L-methionine methyl ester) prevented the PTH-mediated degradation of the transporter, whereas inhibition of the proteasomal pathway (by lactacystin) did not. Moreover it was found (i) that whereas lysosomal inhibitors prevented the PTH-mediated degradation of the transporter they did not prevent the PTH-mediated inhibition of the Na/Pi cotransport and (ii) that treating opossum kidney cells with lysosomal inhibitors led to an increased expression of the transporter without any concomitant increase in the Na/Pi cotransport. Further analysis by subcellular fractionation and morphological techniques showed (i) that the Na/Pi cotransporter is constitutively transported to and degraded within late endosomes/lysosomes and (ii) that PTH leads to the increased degradation of the transporter in late endosomes/lysosomes.
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            Parathyroid hormone and dietary phosphate provoke a lysosomal routing of the proximal tubular Na/Pi-cotransporter type II.

            M Traebert, I Keusch, M Lötscher … (1998)
            A decrease of proximal tubular reabsorption of phosphate (Pi), which can be provoked by parathyroid hormone (PTH) or by a high Pi-diet, has been shown to correlate with a decrease of the number of type II Na/Pi-cotransporters residing in the brush border membrane. While both PTH and a high Pi-diet lead to an internalization of type II cotransporters, the further cellular routing of internalized cotransporters has not been established unequivocally. To prevent lysosomal degradation, rats were treated with leupeptin prior to the injection of PTH or feeding acutely with a high Pi-diet. Kidney cortex were recovered and used for immunohistochemistry. In parallel, brush border membranes and lysosomes were isolated and analyzed by Western blotting. Under both conditions (PTH and high Pi-diet), a strong overlap of internalized type II cotransporters with the late endosomes/lysosomes was observed by immunohistochemistry. In agreement, the content of type II Na/Pi-cotransporters was increased in lysosomes isolated from the corresponding tissues. These results suggest that in proximal tubular cells type II Na/Pi-cotransporters internalized due to the action of PTH and acute high Pi-diet are routed to the lysosomes, and likely do not enter a recycling compartment.
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              A molecular view of proximal tubular inorganic phosphate (Pi) reabsorption and of its regulation.

              H Murer, J Biber (1997)
              In recent years, two mammalian proximal tubular brush border membrane Na/Pi cotransporters (types I and II) have been structurally identified by expression cloning techniques. Oocyte expression studies have shown that only the transport characteristics of the type II transporter correspond to the well-known properties of proximal tubular brush border membrane of Pi transport. In studies on physiological regulation by hormonal and non-hormonal factors a direct involvement and determining role of the type II transporter has been documented. Most interestingly, specific membrane retrieval/insertion phenomena participate in acute (minutes/hours) adjustments of brush border membrane Na/Pi cotransport rates; for chronic (hours/days) alterations also specific resynthesis/degradation processes participate. In pathophysiological alterations (e.g. in X-linked hypophosphataemia and in heavy metal-induced nephrotoxicity) the expression of the type II Na/Pi cotransporters is reduced and explains the observed phosphaturia.
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                Author and article information

                Journal
                Journal ID (publisher-id): KBR
                Journal ID (nlm-ta): Kidney Blood Press Res
                Journal ID (doi): 10.1159/issn.1420-4096
                Title: Kidney and Blood Pressure Research
                Publisher: S. Karger AG
                ISSN (Print): 1420-4096
                ISSN (Electronic): 1423-0143
                Publication date Subscription-year: 2001
                Publication date (Print): 2001
                Publication date (Electronic): 24 January 2001
                Volume: 24
                Issue: 1
                Pages: 1-4
                Affiliations
                Institute of Physiology, University of Zurich, Zurich, Switzerland
                Article
                Publisher ID: 54198 Other ID: Kidney Blood Press Res 2001;24:1–4
                DOI: 10.1159/000054198
                PubMed ID: 11173999
                SO-VID: ccec9c12-5163-4f78-a1aa-0d22262fb13d
                Copyright © © 2001 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Figures: 2, References: 14, Pages: 4
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Type IIa Na/Pi Cotransporter,Phosphoprotein,Phosphorylation
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Type IIa Na/Pi Cotransporter, Phosphoprotein, Phosphorylation

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