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Blood, 1 January 2005, Vol. 105, No. 1, pp. 382-386. Prepublished online as a Blood First Edition Paper on September 7, 2004; DOI 10.1182/blood-2003-11-3755. This Article Full Text (PDF) All Versions of this Article: 2003-11-3755v1 105/1/382    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Rivera, A. Articles by Brugnara, C. Search for Related Content PubMed PubMed Citation Articles by Rivera, A. Articles by Brugnara, C. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 4, 2003 Accepted August 20, 2004 Abnormal regulation of Mg transport via Na/Mg exchange in sickle erythrocytes Alicia Rivera*, Ana Ferreira, Danielle Bertoni, Jose R Romero, and Carlo Brugnara Department of Laboratory Medicine, Children's Hospital, Boston, MA, USA; Department of Pathology, Harvard Medical School, Boston, MA, USA Division of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Boston, MA, USA; Dept. of Medicine, Harvard Medical School, Boston, MA, USA * Corresponding author; email: alicia.rivera{at}childrens.harvard.edu. Erythrocyte magnesium (Mg) deficiency has been demonstrated in sickle cell disease to contribute to erythrocyte dehydration and K loss and thus sickling. No studies have assessed the functional properties of the Na/Mg exchanger in sickle cell disease. Using Mg2+ loaded erythrocytes, we measured Mg2+ efflux induced by extracellular Na+. We estimated that the Na/Mg exchanger had higher maximal velocity, higher affinity for Na+, and lower cooperativity for Mg2+ in sickle than in normal erythrocytes. The activity of the exchanger was markedly decreased by hypotonic and hypertonic conditions in normal erythrocytes but not in sickle erythrocytes. Studies of density-separated erythrocytes showed that the activity of the exchanger decreased as the mean cellular hemoglobin concentration increased in normal but not in sickle erythrocytes. Inhibition of PKC activity by calphostin C and chelerythrine increased the activity of the exchanger in normal but not in sickle erythrocytes. Inhibition of serine/threonine phosphatases did not affect the activity of the exchanger in either normal or sickle erythrocytes. Altogether, these data indicate that Na/Mg exchanger is abnormally regulated in sickle erythrocytes. Therefore, Mg2+ depletion in sickle erythrocytes might be mediated by an upregulated Na/Mg exchanger, possibly by dephosphorylation of the transporter or a closely associated regulator. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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