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Molecular Crowding Limits the Role of Fetal Hemoglobin in Therapy for Sickle Cell Disease
Journal article   Peer reviewed

Molecular Crowding Limits the Role of Fetal Hemoglobin in Therapy for Sickle Cell Disease

Maria Rotter, Alexey Aprelev, Kazuhiko Adachi and Frank A Ferrone
Journal of molecular biology, v 347(5), pp 1015-1023
2005
PMID: 15784260

Abstract

HbS hydroxyurea HbF polymerization kinetics
The dominant assumption central to most treatments for sickle cell anemia has been that replacement of sickle hemoglobin (HbS) by fetal hemoglobin (HbF) would have major clinical benefit. Using laser photolysis, we have measured polymerization kinetics including rates of homogeneous and heterogeneous nucleation on mixtures of 20% and 30% HbF with HbS. We find that the present model for polymerization, including molecular crowding, can accurately predict the rates of such mixtures, by using the single assumption that no significant amount of HbF enters the polymer. The effects of replacing HbS by HbF on the rates of polymer formation are found to be significantly lower than previous measurements appeared to indicate because the impact of the replacement is also highly dependent on the total hemoglobin concentration. This is because the molecular crowding of non-polymerizing HbF offsets substantially the effects of decreasing the concentration of HbS concentration, an effect that increases with concentration. Most strikingly, the demonstrated benefit of hydroxyurea therapy in slowing the kinetics of intracellular polymerization cannot be primarily due to enhanced HbF, but must have some other origin, which could itself represent a promising therapeutic approach.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
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