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      Epidermal Growth Factor Regulates Ca 2+ Uptake in Primary Cultured Renal Proximal Tubule Cells: Involvement of cAMP, PKC and cPLA 2

      a , b , a

      Kidney and Blood Pressure Research

      S. Karger AG

      EGF, Ca2+ uptake, cAMP, PKC, Kidney

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          Abstract

          Epidermal growth factor (EGF) is known to play an important role in modulating renal transport functions. Thus, we investigated the effect of EGF on Ca<sup>2+</sup> uptake and its related signals in the primary cultured rabbit renal proximal tubule cells. EGF (50 ng/ml, 1 h) stimulated Ca<sup>2+</sup> uptake. Its effect was blocked by AG 1478 (an EGF receptor antagonist), genistein or herbimycin A (tyrosine kinase inhibitors). EGF increased intracellular cAMP level and SQ 22536 (an adenylate cyclase inhibitor), Rp-cAMP (a cAMP analogue), or PKI (a protein kinase A inhibitor) blocked the EGF-induced stimulation of Ca<sup>2+</sup> uptake. EGF-induced stimulation of Ca<sup>2+</sup> uptake was also blocked by neomycin or U-73122 (phospholipase C inhibitors), staurosporine, H-7, or bisindolylmaleimide I (protein kinase C inhibitors), nifedipine or methoxyverapamil (L-type Ca<sup>2+</sup> channel blockers). It increased IPs formation by 167 ± 5% compare to control within 90 s. On the other hand, EGF increased [<sup>3</sup>H]-arachidonic acid release, which was significantly blocked by PKC inhibitors. In addition, PGE<sub>2</sub>, one of cyclooxygenase metabolites, and 5,6-EET, one of cytochrome P-450 metabolites, increased Ca<sup>2+</sup> uptake. These results suggest that cAMP, PLC/PKC, and PLA<sub>2</sub> are involved in EGF-induced stimulation of Ca<sup>2+</sup> uptake.

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          Most cited references 8

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          Characterization of primary rabbit kidney cultures that express proximal tubule functions in a hormonally defined medium

          Primary cultures of rabbit-kidney epithelial cells derived from purified proximal tubules were maintained without fibroblast overgrowth in a hormone-supplemented serum-free medium (Medium RK-1). A hormone- deletion study indicated that the primary cultures derived from purified rabbit proximal tubules required all of the three supplements in Medium RK-1 (insulin, transferrin, and hydrocortisone) for optimal growth but did not grow in response to EGF and T3. In contrast, the epithelial cells in primary cultures derived from an unpurified preparation of rabbit kidney tubules and glomeruli grew in response to EGF and T3, as well as insulin, transferrin, and hydrocortisone. These observations suggest that kidney epithelial cells derived from different segments of the nephron grow differently in response to hormones and growth factors. Differentiated functions of the primary cultures derived from proximal tubules were examined. Multicellular domes were observed, indicative of transepithelial solute transport by the monolayers. The proximal tubule cultures also accumulated alpha- methylglucoside (alpha-MG) against a concentration gradient. However, little or no alpha-MG accumulation was observed in the absence of Na+. Metabolic inhibitor studies also indicated that alpha-MG uptake by the primaries is an energy-dependent process, and depends upon the activity of the Na+/K+ ATPase. Phlorizin at 0.1 mM significantly inhibited 1 mM alpha-MG uptake whereas 0.1 mM phloretin did not have a significant inhibitory effect. Similar observations have been made concerning the Na+-dependent sugar-transport system located on the lumenal side of the proximal tubule, whereas the Na+-independent sugar transporter on the peritubular side is more sensitive to inhibition by phloretin than phlorizin. The cultures also exhibited PTH-sensitive cyclic AMP synthesis and brush-border enzymes typical of proximal cells. However, the activities of the enzymes leucine aminopeptidase, alkaline phosphatase, and gamma-glutamyl-transpeptidase were lower in the cultures than in purified proximal-tubule preparations from which they are derived.
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            High glucose inhibits renal proximal tubule cell proliferation and involves PKC, oxidative stress, and TGF-beta 1.

             Paul Han,  M. Park,  T. J. Kim (2001)
            The alteration of renal cell growth is one of the early abnormalities in the diabetic nephropathy. However, the effects of high glucose and its action mechanism in renal proximal tubule cell (PTC) proliferation have not been elucidated. The effects of 25 mmol/L glucose on cell proliferation, thymidine, and leucine incorporation, cell cycle, and lipid peroxide formation were examined in the primary cultured renal PTCs. Glucose 25 mmol/L inhibited [3H]-thymidine incorporation and decreased cell growth. However, it increased [3H]-leucine incorporation and protein content. Furthermore, 25 mmol/L glucose increased lipid peroxide formation. These effects of glucose were blocked by antioxidants, vitamin E, N-acetylcystein, or taurine. Staurosporine and H-7 totally blocked 25 mmol/L glucose-induced lipid peroxide formation and had an inhibitory effect on [3H]-thymidine incorporation. Indeed, 25 mmol/L glucose increased the translocation of protein kinase C (PKC) from cytosolic fraction to membrane fraction. In addition, high glucose increased the secretion of transforming growth factor-beta1 (TGF-beta 1) via the PKC-oxidative stress pathway, and TGF-beta 1 inhibited [3H]-thymidine incorporation in a dose-dependent manner. High glucose inhibits renal PTC proliferation via PKC, oxidative stress, and the TGF-beta 1 signaling pathway.
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              Stimulation of protein kinase C recruits covert calcium channels in Aplysia bag cell neurons.

               J. Strong,  A Fox,  R Tsien (2015)
              The modulation of voltage-activated calcium currents by protein kinases provides excitable cells with a mechanism for regulating their electrical behaviour. At the single channel level, modulation of calcium current has, to date, been characterized only in cardiac muscle, where beta-adrenergic agonists, acting through cyclic AMP-dependent protein kinase, enhance the calcium current by increasing channel availability and opening. We now report that enhancement of calcium current in the peptidergic bag cell neurons of Aplysia by protein kinase C occurs through a different mechanism, the recruitment of a previously covert class of calcium channel. Under control conditions, bag cell neurons contain only one class of voltage-activated calcium channel with a conductance of approximately 12 pS. After exposure to agents that activate protein kinase C, these neurons also express a second class of calcium channel with a different unitary conductance (approximately 24 pS) that is never seen in untreated cells.
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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2003
                2003
                29 July 2003
                : 26
                : 3
                : 155-164
                Affiliations
                aDepartment of Veterinary Physiology, College of Veterinary Medicine, Biotechnology Research Institute, Chonnam National University, Gwangju, and bCollege of Veterinary Medicine, Chonbuk National University, Jeonju, Korea
                Article
                71881 Kidney Blood Press Res 2003;26:155–164
                10.1159/000071881
                12886043
                © 2003 S. Karger AG, Basel

                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.

                Page count
                Figures: 8, Tables: 1, References: 47, Pages: 10
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/71881
                Categories
                Original Paper

                Cardiovascular Medicine, Nephrology

                Ca2+ uptake, cAMP, PKC, EGF, Kidney

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