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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 (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 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 Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 13, 2004 Accepted May 25, 2004 KCl Cotransport Mediates Abnormal, Sulfhydryl-Dependent Volume Regulation in Sickle Reticulocytes Clinton H Joiner*, R K Rettig, Maorong Jiang, and Robert S Franco Cincinnati Comprehensive Sickle Cell Center, Cincinnati, OH, USA; Division of Hematology/Oncology, Children's Hospital Medical Center, Cincinnati, OH, USA Cincinnati Comprehensive Sickle Cell Center, Cincinnati, OH, USA; Department of Internal Medicine, Division of Medical Hematology/Oncology, University of Cincinnati, Cincinnati, OH, USA * Corresponding author; email: clint.joiner{at}cchmc.org. KCl cotransport (KCC) activation by cell swelling and pH was compared in sickle (SS) and normal (AA) red blood cells (RBC). KCC fluxes had the same relationship to MCHC in SS and AA RBC when normalized to the maximal volume-stimulated (VSmax) flux (MCHC < 27 gm/dl). Acid-stimulated (pH 6.9) KCC flux in SS RBC was 60-70% of VSmax KCC, versus 20% in AA RBC. Density gradients were used to track changes in reticulocyte MCHC during KCC-mediated regulatory volume decrease (RVD). Swelling to MCHC 26 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 RBC by one third, but did not alter swelling-induced RVD. DTT lowered acid-activated KCC in SS RBC by 50%, and diminished acid-induced RVD in SS reticulocytes. Thus, swelling activation of KCC is normal in SS RBC, but KCC-mediated RVD produces higher MCHC in SS than AA reticulocytes. Acid activation of KCC is exaggerated in SS RBC 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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