Delayed Onset of Hemolytic Anemia in
CBA-Pk-1slc/Pk-1slc Mice With a Point
Mutation of the Gene Encoding Red Blood Cell Type Pyruvate Kinase
Kumiko Tsujino,
Hitoshi Kanno,
Koji Hashimoto,
Hisaichi Fujii,
Tomoko Jippo,
Eiichi Morii,
Young-Mi Lee,
Hidekazu Asai,
Shiro Miwa, and
Yukihiko Kitamura
From the Department of Pathology, Osaka University Medical School,
Suita, Osaka; Okinaka Memorial Institute for Medical Research,
Minato-ku, Tokyo; the Department of Blood Transfusion Medicine, Tokyo
Women's Medical College, Shinjyuku-ku, Tokyo; and Japan SLC Co Ltd,
Hamamatsu, Shizuoka, Japan.
The Pk-1slc gene encodes a mutant red blood cell
(RBC) type pyruvate kinase (PK), and adult
CBA-Pk-1slc/Pk-1slc mice show a severe
nonspherocytic hemolytic anemia. However, the number of RBCs and the
proportion of reticulocytes were comparable between neonatal
CBA-Pk-1slc/Pk-1slc mice and control
-+/+ mice. Since the age-dependent increase of RBCs was much
greater in CBA-+/+ mice than in
CBA-Pk-1slc/Pk-1slc mice, significant
anemia was observed in the latter mice on day 14 after birth. The
increase of RBCs in CBA-+/+ mice was due to the prolongation of
their survival time. The half life of RBCs increased in CBA-+/+
mice with ages, but it decreased in
CBA-Pk-1slc/Pk-1slc mice. The
relatively longer half life of RBCs in neonatal
CBA-Pk-1slc/Pk-1slc mice appeared to be
due to the delayed switching from M2-type PK that are expressed by
undifferentiated erythroid precursor cells to RBC-type PK that are
expressed by mature RBCs.
Blood, Vol. 91 No. 6 (March 15), 1998:
pp. 2169-2174
© 1998 by The American Society of Hematology.
