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Blood, 1 April 2001, Vol. 97, No. 7, pp. 2151-2158
RED CELLS
Reduced oxidative-stress response in red blood cells from
p45NFE2-deficient mice
Jefferson Y. Chan,
Mandy Kwong,
Margaret Lo,
Renee Emerson, and
Frans A. Kuypers
From the Department of Laboratory Medicine, University
of California, San Francisco; and Children's Hospital Oakland Research
Institute, Oakland, CA.
p45NF-E2 is a member of the cap `n' collar (CNC)-basic leucine
zipper family of transcriptional activators that is expressed at high
levels in various types of blood cells. Mice deficient in p45NF-E2 that
were generated by gene targeting have high mortality from bleeding
resulting from severe thrombocytopenia. Surviving p45nf-e2 / adults have mild anemia
characterized by hypochromic red blood cells (RBCs), reticulocytosis,
and splenomegaly. Erythroid abnormalities in
p45nf-e2/ animals were previously
attributed to stress erythropoiesis caused by chronic bleeding and,
possibly, ineffective erythropoiesis. Previous studies suggested that
CNC factors might play essential roles in regulating expression of
genes that protect cells against oxidative stress. In this study, we
found that p45NF-E2-deficient RBCs have increased levels of reactive
oxygen species and an increased susceptibility to
oxidative-stress-induced damage. Deformability of p45NF-E2-deficient
RBCs was markedly reduced with oxidative stress, and mutant cells
had a reduced life span. One possible reason for increased sensitivity
to oxidative stress is that catalase levels were reduced in mutant
RBCs. These findings suggest a role for p45NF-E2 in the
oxidative-stress response in RBCs and indicate that p45NF-E2 deficiency
contributes to the anemia in
p45nf-e2/ mice.
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