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Blood, 1 March 2002, Vol. 99, No. 5, pp. 1817-1824
RED CELLS
Failure of red blood cell maturation in mice with defects in the
high-density lipoprotein receptor SR-BI
Teresa M. Holm,
Anne Braun,
Bernardo L. Trigatti,
Carlo Brugnara,
Masa Sakamoto,
Monty Krieger, and
Nancy C. Andrews
From the Division of Hematology/Oncology, Children's
Hospital; the Department of Pediatrics, Harvard Medical School; and the
Howard Hughes Medical Institute, Boston, MA; and the Department of
Biology, Massachusetts Institute of Technology, Cambridge, MA.
Mammalian erythrocytes undergo a unique maturation process in which
they discard their nuclei and organelles and assume a flexible
biconcave shape. We found that altered plasma lipoprotein metabolism
can profoundly influence these events. Abnormal erythrocyte morphology
was observed in hypercholesterolemic mice lacking the high-density
lipoprotein receptor SR-BI. This was exacerbated by feeding mice a
high-cholesterol diet or, more dramatically, by inactivating the
apolipoprotein E gene. Erythrocytes from
SR-BI //apolipoprotein
E/ mice and SR-BI/
mice that were fed cholesterol had markedly increased membrane cholesterol. Their morphology appeared immature, with macrocytosis, irregular shape, and large autophagolysosomes. Autophagolysosomes from
SR-BI//apolipoprotein
E/ erythrocytes were expelled when the
erythrocytes were transfused into wild-type animals or incubated in
vitro with normolipidemic serum or the cholesterol-sequestering agent
methyl cyclodextrin. We propose that autophagocytosis and phagolysosome
expulsion are essential steps in erythroid maturation and that
expulsion is inhibited in the presence of markedly increased cellular cholesterol.
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