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Regulation of transferrin receptors by iron in human erythroblasts
Author(s) -
Abe Yasunobu,
Muta Koichiro,
Nishimura Junji,
Nawata Hajime
Publication year - 1992
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830400406
Subject(s) - transferrin , erythroblast , transferrin receptor , hemin , receptor , hemoglobin , microbiology and biotechnology , in vivo , chemistry , messenger rna , biology , heme , biochemistry , gene , enzyme , haematopoiesis , genetics , stem cell
We investigated the regulatory mechanism of human erythroblast transferrin receptors (Tf.R) under conditions of iron deprivation and iron loading. Treatment of erythroblasts with an iron chelator, desferrioxamine, induced an increase in surface Tf.R number associated with an elevation of biosynthetic rate and the mRNA level of Tf.R. Reduced cellular iron pool increased the Tf.R number by altering the level of mRNA, as in nonhemoglobinproducing cells. Although treatment of erythroblasts with hemin induced a decrease in the biosynthetic rate and in the level of mRNA, the number of surface Tf.R did not decrease. This phenomenon may explain the fact that a high level of serum iron has no influence on the surface Tf.R number in vivo, as we reported previously. We suggest the existence of a regulatory mechanism specific for hemoglobin‐producing cells that keeps surface Tf.R expression constant despite iron loading. © 1992 Wiley‐Liss, Inc.