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Research Article Free access | 10.1172/JCI113640

Decreased membrane mechanical stability and in vivo loss of surface area reflect spectrin deficiencies in hereditary spherocytosis.

J A Chasis, P Agre, and N Mohandas

Department of Medicine and Laboratory Medicine, University of California, San Francisco 94143.

Find articles by Chasis, J. in: PubMed | Google Scholar

Department of Medicine and Laboratory Medicine, University of California, San Francisco 94143.

Find articles by Agre, P. in: PubMed | Google Scholar

Department of Medicine and Laboratory Medicine, University of California, San Francisco 94143.

Find articles by Mohandas, N. in: PubMed | Google Scholar

Published August 1, 1988 - More info

Published in Volume 82, Issue 2 on August 1, 1988
J Clin Invest. 1988;82(2):617–623. https://doi.org/10.1172/JCI113640.
© 1988 The American Society for Clinical Investigation
Published August 1, 1988 - Version history
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Abstract

Whereas marked variations in the clinical manifestations of hereditary spherocytosis have long been recognized, we have only recently begun to define the molecular basis for this heterogeneity. An important unanswered question is whether decreased spectrin results in reduced membrane mechanical stability, and if this reduction in membrane mechanical stability can be related to in vivo surface area loss. Using the ektacytometer, we quantitated membrane surface area and stability in erythrocytes from 18 individuals with hereditary spherocytosis and deficiencies of spectrin (30-80% of normal spectrin level). Membrane mechanical stability was reduced and the magnitude of the reductions correlated with the spectrin content. Moreover, the reductions in mechanical stability correlated with in vivo loss of membrane surface area. These data indicate that decreased spectrin content results in reduced membrane mechanical stability and surface area loss in vivo. We conclude that partial deficiencies of spectrin, reductions in membrane mechanical stability, and loss of membrane surface area are directly related and are major features determining the heterogeneous clinical manifestations of hereditary spherocytosis.

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