Rs. Franco et al., FETAL HEMOGLOBIN AND POTASSIUM IN ISOLATED TRANSFERRIN RECEPTOR-POSITIVE DENSE SICKLE RETICULOCYTES, Blood, 84(6), 1994, pp. 2013-2020
A subset of sickle cells have an increased density at the reticulocyte
stage of development, indicating that they are either abnormally dens
e upon release from the bone marrow or become dense quickly in the cir
culation. These cells are of interest because they most likely have se
verely disrupted cation regulation and a short lifespan. Based on the
distribution of fetal hemoglobin (HbF) in the density fractions of sic
kle red blood cells (RBCs) and in vitro studies of cellular K+ loss, i
t seems likely that HbF content is an important in vivo determinant of
dense cell formation. In this study, we tested the hypothesis that yo
ung, dense cells have low HbF content. Sickle RBCs were first separate
d into light and dense fractions. Reticulocytes were isolated from unf
ractionated cells and from each density fraction with an immunomagneti
c technique directed against transferrin receptors (TfR) and assayed f
or the percentage of HbF and K+/Hb ratio. TfR(+) reticulocytes isolate
d from unfractionated cells had a much lower HbF content when compared
with all the unfractionated RBCs. This is most likely caused by enric
hment of F cells because of a longer circulation life span. Heavy TfR(
+) reticulocytes had a K+/Hb ratio similar to that measured in the ent
ire dense population and contained very low levels of HbF, averaging 2
.5% of the level in all RBCs, 11.7% of the level in all TfR(+) reticul
ocytes, and 4.0% of the level in all dense RBCs. These findings sugges
t that TfR(+) dense cells derive predominantly from non-F cells. Furth
ermore, the amount of HbF in the circulating dense cells suggests that
many of these cells do not derive from the TfR(+) dense cells. (C) 19
94 by The American Society of Hematology.