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Blood, 1 November 2004, Vol. 104, No. 9, pp. 2954-2960. Prepublished online as a Blood First Edition Paper on July 8, 2004; DOI 10.1182/blood-2004-01-0112. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-01-0112v1 104/9/2954    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Joiner, C. H. Articles by Franco, R. S. Search for Related Content PubMed PubMed Citation Articles by Joiner, C. H. Articles by Franco, R. S. Related Collections Red Cells Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS KCl cotransport mediates abnormal sulfhydryl-dependent volume regulation in sickle reticulocytes Clinton H. Joiner, R. Kirk Rettig, Maorong Jiang, and Robert S. Franco From the Cincinnati Comprehensive Sickle Cell Center, Cincinnati, OH; Division of Hematology/Oncology, Children's Hospital Medical Center, Cincinnati, OH; and Division of Medical Hematology/Oncology, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH. KCl cotransport (KCC) activation by cell swelling and pH was compared in sickle (SS) and normal (AA) red blood cells (RBCs). KCC fluxes had the same relationship to mean corpuscular hemoglobin concentration (MCHC) in SS and AA RBCs when normalized to the maximal volume-stimulated (VSmax) flux (MCHC < 270 g/L [27 g/dL]). Acid-stimulated (pH 6.9) KCC flux in SS RBCs was 60% to 70% of VSmax KCC versus 20% in AA RBCs. Density gradients were used to track changes in reticulocyte MCHC during KCC-mediated regulatory volume decrease (RVD). Swelling to MCHC of 260 g/L (26 g/dL) produced Cl-dependent RVD that resulted in higher MCHC in SS than AA reticulocytes. In acid pH, RVD was also greater in SS than AA reticulocytes. Sulfhydryl reduction by dithiothreitol (DTT) lowered VSmax KCC flux in AA and SS RBCs by one third but did not alter swelling-induced RVD. DTT lowered acid-activated KCC in SS RBCs by 50% and diminished acid-induced RVD in SS reticulocytes. Thus, swelling activation of KCC is normal in SS RBCs but KCC-mediated RVD produces higher MCHC in SS than AA reticulocytes. Acid activation of KCC is exaggerated in SS RBCs and causes dehydration in SS reticulocytes. KCC response to acid stimulation was mitigated by DTT, suggesting that it arises from sulfhydryl oxidation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. H. Joiner, R. Kirk Rettig, M. Jiang, M. Risinger, and R. S. Franco Urea stimulation of KCl cotransport induces abnormal volume reduction in sickle reticulocytes Blood, February 15, 2007; 109(4): 1728 - 1735. [Abstract] [Full Text] [PDF] C. H. Joiner, R. K. Rettig, M. Palascak, A. Sheriff, R. M. Cohen, and R. S. Franco Mature Sickle and Normal Red Cells Exhibit Regulatory Volume Decrease Activated by Urea and Mediated by KCl Cotransport. Blood (ASH Annual Meeting Abstracts), November 16, 2005; 106(11): 2321 - 2321. [Abstract]

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